Hiv fusion inhibitors. Medical search

Inhibitors of the fusion of HIV to host cells, preventing viral entry. This includes compounds that block attachment of HIV ENVELOPE PROTEIN GP120 to CD4 RECEPTORS.

Transmembrane envelope protein of the HUMAN IMMUNODEFICIENCY VIRUS which is encoded by the HIV env gene. It has a molecular weight of 41,000 and is glycosylated. The N-terminal part of gp41 is thought to be involved in CELL FUSION with the CD4 ANTIGENS of T4 LYMPHOCYTES, leading to syncytial formation. Gp41 is one of the most common HIV antigens detected by IMMUNOBLOTTING.

The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.

Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.

The entering of cells by viruses following VIRUS ATTACHMENT. This is achieved by ENDOCYTOSIS, by direct MEMBRANE FUSION of the viral membrane with the CELL MEMBRANE, or by translocation of the whole virus across the cell membrane.

The adherence and merging of cell membranes, intracellular membranes, or artificial membranes to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes.

Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).

The ability of viruses to resist or to become tolerant to chemotherapeutic agents or antiviral agents. This resistance is acquired through gene mutation.

Fusion of somatic cells in vitro or in vivo, which results in somatic cell hybridization.

Agents used to treat AIDS and/or stop the spread of the HIV infection. These do not include drugs used to treat symptoms or opportunistic infections associated with AIDS.

The molecular designing of drugs for specific purposes (such as DNA-binding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis.

Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.

The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.

Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

Proteins, usually glycoproteins, found in the viral envelopes of a variety of viruses. They promote cell membrane fusion and thereby may function in the uptake of the virus by cells.

Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.

Dissection of human immunodeficiency virus type 1 entry with neutralizing antibodies to gp41 fusion intermediates. (1/304)

Human immunodeficiency virus type 1 (HIV-1) entry requires conformational changes in the transmembrane subunit (gp41) of the envelope glycoprotein (Env) involving transient fusion intermediates that contain exposed coiled-coil (prehairpin) and six-helix bundle structures. We investigated the HIV-1 entry mechanism and the potential of antibodies targeting fusion intermediates to block Env-mediated membrane fusion. Suboptimal temperature (31.5 degrees C) was used to prolong fusion intermediates as monitored by confocal microscopy. After transfer to 37 degrees C, these fusion intermediates progressed to syncytium formation with enhanced kinetics compared with effector-target (E/T) cell mixtures that were incubated only at 37 degrees C. gp41 peptides DP-178, DP-107, and IQN17 blocked fusion more efficiently (5- to 10-fold-lower 50% inhibitory dose values) when added to E/T cells at the suboptimal temperature prior to transfer to 37 degrees C. Rabbit antibodies against peptides modeling the N-heptad repeat or the six-helix bundle of gp41 blocked fusion and viral infection at 37 degrees C only if preincubated with E/T cells at the suboptimal temperature. Similar fusion inhibition was observed with human six-helix bundle-specific monoclonal antibodies. Our data demonstrate that antibodies targeting gp41 fusion intermediates are able to bind to gp41 and arrest fusion. They also indicate that six-helix bundles can form prior to fusion and that the lag time before fusion occurs may include the time needed to accumulate preformed six-helix bundles at the fusion site. (+info)

Human CD38 interferes with HIV-1 fusion through a sequence homologous to the V3 loop of the viral envelope glycoprotein gp120. (2/304)

CD38 is a progression marker in HIV-1 infection, it displays lateral association with CD4, and down-modulates gp120/CD4 binding. The aim of this study was to elucidate the mechanism behind the interplay between CD4, CD38, and HIV-1. We used mouse cell transfectants expressing human CD4 and either CD38 or other CD4-associated molecules to show that CD38 specifically inhibits gp120/CD4 binding. Human cell transfectants expressing truncated forms of CD38 and bioinformatic analysis were used to map the anti-HIV activity and show that it is concentrated in the membrane-proximal region. This region displayed significant sequence-similarity with the V3 loop of the HIV-1 gp120 glycoprotein. In line with this similarity, synthetic soluble peptides derived from this region reproduced the anti-HIV effects of full-length CD38 and inhibited HIV-1 and HIV-2 primary isolates from different subtypes and with different coreceptor use. A multiple-branched peptide construct presenting part of the sequence of the V3-like region potently and selectively inhibited HIV-1 replication in the nanomolar range. Conversely, a deletion in the V3-like region abrogated the anti-HIV-1 activity of CD38 and its lateral association with CD4. These findings may provide new insights into the early events of HIV-1 fusion and strategies to intervene. (+info)

Enfuvirtide, an HIV-1 fusion inhibitor, for drug-resistant HIV infection in North and South America. (3/304)

BACKGROUND: The T-20 vs. Optimized Regimen Only Study 1 (TORO 1) was a randomized, open-label, phase 3 study of enfuvirtide (T-20), a human immunodeficiency virus type 1 (HIV-1) fusion inhibitor. METHODS: Patients from 48 sites in the United States, Canada, Mexico, and Brazil with at least six months of previous treatment with agents in three classes of antiretroviral drugs, resistance to drugs in these classes, or both, and with at least 5000 copies of HIV-1 RNA per milliliter of plasma were randomly assigned in a 2:1 ratio to receive enfuvirtide plus an optimized background regimen of three to five antiretroviral drugs or such a regimen alone (control group). The primary efficacy end point was the change in the plasma HIV-1 RNA level from base line to week 24. RESULTS: A total of 501 patients underwent randomization, and 491 received at least one dose of study drug and had at least one measurement of plasma HIV-1 RNA after treatment began. The two groups were balanced in terms of the median base-line HIV-1 RNA level (5.2 log10 copies per milliliter in both groups), median CD4+ cell count (75.5 cells per cubic millimeter in the enfuvirtide group, and 87.0 cells per cubic millimeter in the control group), demographic characteristics, and previous antiretroviral therapy. At 24 weeks, the least-squares mean change from base line in the viral load (intention-to-treat, last observation carried forward) was a decrease of 1.696 log10 copies per milliliter in the enfuvirtide group, and a decrease of 0.764 log10 copies per milliliter in the control group (P<0.001). The mean increases in CD4+ cell count were 76 cells per cubic millimeter and 32 cells per cubic millimeter, respectively (P<0.001). Reactions at the site of the injections were reported by 98 percent of patients receiving enfuvirtide. There were more cases of pneumonia in the enfuvirtide group than in the control group. CONCLUSIONS: The addition of enfuvirtide to an optimized antiretroviral regimen provided significant antiretroviral and immunologic benefit through 24 weeks in patients who had previously received multiple antiretroviral drugs and had multidrug-resistant HIV-1 infection. (+info)

Efficacy of enfuvirtide in patients infected with drug-resistant HIV-1 in Europe and Australia. (4/304)

BACKGROUND: The T-20 vs. Optimized Regimen Only Study 2 (TORO 2) compared the efficacy and safety of 24 weeks of treatment with the fusion inhibitor enfuvirtide in combination with an optimized background antiretroviral regimen with the efficacy and safety of the optimized background regimen alone. METHODS: The patients had previous treatment with each of the three classes of antiretroviral drugs, documented resistance to each class, or both and a plasma level of human immunodeficiency virus type 1 (HIV-1) RNA of at least 5000 copies per milliliter. They were randomly assigned in a 2:1 ratio to receive either enfuvirtide (90 mg twice daily) plus a background regimen optimized with the aid of resistance testing (enfuvirtide group) or the background regimen alone (control group). RESULTS: Of the 512 patients who underwent randomization, 335 in the enfuvirtide group and 169 in the control group received at least one dose of study medication and had at least one follow-up measurement of plasma HIV-1 RNA. The median base-line plasma HIV-1 RNA level was 5.1 log10 copies per milliliter in both groups. The median CD4+ cell count was 98.0 cells per cubic millimeter in the enfuvirtide group and 101.5 cells per cubic millimeter in the control group. Patients had a median of seven years of previous treatment and had received a median of 12 antiretroviral drugs. The background regimen comprised a mean of four antiretroviral drugs in both groups. At 24 weeks, the least-squares mean change from base line in the plasma viral load (intention-to-treat, last observation carried forward) was a decrease of 1.429 log10 copies per milliliter in the enfuvirtide group and a decrease of 0.648 log10 copies per milliliter in the control group, a difference of 0.781 log10 copies per milliliter (P<0.001). The mean increase in the CD4+ cell count was greater in the enfuvirtide group (65.5 cells per cubic millimeter) than in the control group (38.0 cells per cubic millimeter, P=0.02). CONCLUSIONS: The addition of enfuvirtide to an optimized background regimen provided significant viral suppression and immunologic benefit over a 24-week period in HIV-1-infected patients who had previously received multiple antiretroviral drugs. (+info)

A small molecule HIV-1 inhibitor that targets the HIV-1 envelope and inhibits CD4 receptor binding. (5/304)

BMS-378806 is a recently discovered small molecule HIV-1 inhibitor that blocks viral entrance to cells. The compound exhibits potent inhibitory activity against a panel of R5-(virus using the CCR5 coreceptor), X4-(virus using the CXCR4 coreceptor), and R5/X4 HIV-1 laboratory and clinical isolates of the B subtype (median EC50 of 0.04 microM) in culture assays. BMS-378806 is selective for HIV-1 and inactive against HIV-2, SIV and a panel of other viruses, and exhibits no significant cytotoxicity in the 14 cell types tested (concentration for 50% reduction of cell growth, >225 microM). Mechanism of action studies demonstrated that BMS-378806 binds to gp120 and inhibits the interactions of the HIV-1 envelope protein to cellular CD4 receptors. Further confirmation that BMS-378806 targets the envelope in infected cells was obtained through the isolation of resistant variants and the mapping of resistance substitutions to the HIV-1 envelope. In particular, two substitutions, M426L and M475I, are situated in the CD4 binding pocket of gp120. Recombinant HIV-1 carrying these two substitutions demonstrated significantly reduced susceptibility to compound inhibition. BMS-378806 displays many favorable pharmacological traits, such as low protein binding, minimal human serum effect on anti-HIV-1 potency, good oral bioavailability in animal species, and a clean safety profile in initial animal toxicology studies. Together, the data show that BMS-378806 is a representative of a new class of HIV inhibitors that has the potential to become a valued addition to our current armamentarium of antiretroviral drugs. (+info)

The entry of entry inhibitors: a fusion of science and medicine. (6/304)

For HIV-1 to enter a cell, its envelope protein (Env) must sequentially engage CD4 and a chemokine coreceptor, triggering conformational changes in Env that ultimately lead to fusion between the viral and host cell membranes. Each step of the virus entry pathway is a potential target for novel antiviral agents termed entry inhibitors. A growing number of entry inhibitors are under clinical development, with one having already been licensed by the Food and Drug Administration. With the emergence of virus strains that are largely resistant to existing reverse transcriptase and protease inhibitors, the development of entry inhibitors comes at an opportune time. Nonetheless, because all entry inhibitors target in some manner the highly variable Env protein of HIV-1, there are likely to be challenges in their efficient application that are unique to this class of drugs. Env density, receptor expression levels, and differences in affinity and receptor presentation are all factors that could influence the clinical response to this promising class of new antiviral agents. (+info)

Putative role of membranes in the HIV fusion inhibitor enfuvirtide mode of action at the molecular level. (7/304)

Partition of the intrinsically fluorescent HIV fusion inhibitor enfuvirtide into lipidic membranes is relatively high (Delta G =6.6 kcal x mol(-1)) and modulated by cholesterol. A shallow position in the lipidic matrix makes it readily available for interaction with gp41. No conformational energetic barrier prevents enfuvirtide from being active in both aqueous solution and lipidic membranes. Lipidic membranes may play a key role in the enfuvirtide biochemical mode of action. (+info)

Enfuvirtide (T-20): a novel human immunodeficiency virus type 1 fusion inhibitor. (8/304)

The development of highly active antiretroviral therapy has improved life expectancy and reduced progression to acquired immunodeficiency syndrome in human immunodeficiency virus (HIV)-infected patients. However, resistance to currently available classes of antiretroviral drugs has become a problem, limiting the options for patients with advanced disease who have been heavily treated. Enfuvirtide (T-20; ENF), a synthetic peptide, is the first of a new class of antiretrovirals that block entry of virus into host cells. ENF interferes with conformational changes required for membrane fusion and injection of virus into the host cell. Optimal treatment of HIV infection will likely require combinations of drugs that target novel stages of HIV type 1 entry and replication. (+info)

HIV Fusion Inhibitors are a type of antiretroviral medication used in the treatment and management of HIV infection. They work by preventing the virus from entering and infecting CD4 cells, which are a type of white blood cell that plays a crucial role in the body's immune response.

Fusion inhibitors bind to the gp41 protein on the surface of the HIV envelope, preventing it from undergoing conformational changes necessary for fusion with the host cell membrane. This inhibits the virus from entering and infecting the CD4 cells, thereby reducing the viral load in the body and slowing down the progression of the disease.

Examples of HIV Fusion Inhibitors include enfuvirtide (T-20) and ibalizumab (TMB-355). These medications are usually used in combination with other antiretroviral drugs as part of a highly active antiretroviral therapy (HAART) regimen. It's important to note that HIV fusion inhibitors must be administered parenterally, typically by injection, due to their large size and poor oral bioavailability.

HIV Envelope Protein gp41 is a transmembrane protein that forms a part of the HIV envelope complex. It plays a crucial role in the viral fusion process, where it helps the virus to enter and infect the host cell. The "gp" stands for glycoprotein, indicating that the protein contains carbohydrate chains. The number 41 refers to its molecular weight, which is approximately 41 kilodaltons.

The gp41 protein exists as a trimer on the surface of the viral envelope and interacts with the host cell membrane during viral entry. It contains several functional domains, including an N-terminal fusion peptide, two heptad repeat regions (HR1 and HR2), a transmembrane domain, and a cytoplasmic tail. During viral fusion, the gp41 protein undergoes significant conformational changes, allowing the fusion peptide to insert into the host cell membrane. The HR1 and HR2 regions then interact to form a six-helix bundle structure, which brings the viral and host cell membranes together, facilitating membrane fusion and viral entry.

The gp41 protein is an important target for HIV vaccine development and antiretroviral therapy. Neutralizing antibodies that recognize and bind to specific epitopes on the gp41 protein can prevent viral entry and infection, while small molecule inhibitors that interfere with the formation of the six-helix bundle structure can also block viral fusion and replication.

HIV-1 (Human Immunodeficiency Virus type 1) is a species of the retrovirus genus that causes acquired immunodeficiency syndrome (AIDS). It is primarily transmitted through sexual contact, exposure to infected blood or blood products, and from mother to child during pregnancy, childbirth, or breastfeeding. HIV-1 infects vital cells in the human immune system, such as CD4+ T cells, macrophages, and dendritic cells, leading to a decline in their numbers and weakening of the immune response over time. This results in the individual becoming susceptible to various opportunistic infections and cancers that ultimately cause death if left untreated. HIV-1 is the most prevalent form of HIV worldwide and has been identified as the causative agent of the global AIDS pandemic.

A peptide fragment is a short chain of amino acids that is derived from a larger peptide or protein through various biological or chemical processes. These fragments can result from the natural breakdown of proteins in the body during regular physiological processes, such as digestion, or they can be produced experimentally in a laboratory setting for research or therapeutic purposes.

Peptide fragments are often used in research to map the structure and function of larger peptides and proteins, as well as to study their interactions with other molecules. In some cases, peptide fragments may also have biological activity of their own and can be developed into drugs or diagnostic tools. For example, certain peptide fragments derived from hormones or neurotransmitters may bind to receptors in the body and mimic or block the effects of the full-length molecule.

Virus internalization, also known as viral entry, is the process by which a virus enters a host cell to infect it and replicate its genetic material. This process typically involves several steps:

1. Attachment: The viral envelope proteins bind to specific receptors on the surface of the host cell.
2. Entry: The virus then enters the host cell through endocytosis or membrane fusion, depending on the type of virus.
3. Uncoating: Once inside the host cell, the viral capsid is removed, releasing the viral genome into the cytoplasm.
4. Replication: The viral genome then uses the host cell's machinery to replicate itself and produce new viral particles.

It's important to note that the specific mechanisms of virus internalization can vary widely between different types of viruses, and are an active area of research in virology and infectious disease.

Membrane fusion is a fundamental biological process that involves the merging of two initially separate lipid bilayers, such as those surrounding cells or organelles, to form a single continuous membrane. This process plays a crucial role in various physiological events including neurotransmitter release, hormone secretion, fertilization, viral infection, and intracellular trafficking of proteins and lipids. Membrane fusion is tightly regulated and requires the participation of specific proteins called SNAREs (Soluble NSF Attachment Protein REceptors) and other accessory factors that facilitate the recognition, approximation, and merger of the membranes. The energy required to overcome the repulsive forces between the negatively charged lipid headgroups is provided by these proteins, which undergo conformational changes during the fusion process. Membrane fusion is a highly specific and coordinated event, ensuring that the correct membranes fuse at the right time and place within the cell.

HIV (Human Immunodeficiency Virus) infection is a viral illness that progressively attacks and weakens the immune system, making individuals more susceptible to other infections and diseases. The virus primarily infects CD4+ T cells, a type of white blood cell essential for fighting off infections. Over time, as the number of these immune cells declines, the body becomes increasingly vulnerable to opportunistic infections and cancers.

HIV infection has three stages:

1. Acute HIV infection: This is the initial stage that occurs within 2-4 weeks after exposure to the virus. During this period, individuals may experience flu-like symptoms such as fever, fatigue, rash, swollen glands, and muscle aches. The virus replicates rapidly, and the viral load in the body is very high.
2. Chronic HIV infection (Clinical latency): This stage follows the acute infection and can last several years if left untreated. Although individuals may not show any symptoms during this phase, the virus continues to replicate at low levels, and the immune system gradually weakens. The viral load remains relatively stable, but the number of CD4+ T cells declines over time.
3. AIDS (Acquired Immunodeficiency Syndrome): This is the most advanced stage of HIV infection, characterized by a severely damaged immune system and numerous opportunistic infections or cancers. At this stage, the CD4+ T cell count drops below 200 cells/mm3 of blood.

It's important to note that with proper antiretroviral therapy (ART), individuals with HIV infection can effectively manage the virus, maintain a healthy immune system, and significantly reduce the risk of transmission to others. Early diagnosis and treatment are crucial for improving long-term health outcomes and reducing the spread of HIV.

Drug resistance, viral, refers to the ability of a virus to continue replicating in the presence of antiviral drugs that are designed to inhibit or stop its growth. This occurs when the virus mutates and changes its genetic makeup in such a way that the drug can no longer effectively bind to and inhibit the function of its target protein, allowing the virus to continue infecting host cells and causing disease.

Viral drug resistance can develop due to several factors, including:

1. Mutations in the viral genome that alter the structure or function of the drug's target protein.
2. Changes in the expression levels or location of the drug's target protein within the virus-infected cell.
3. Activation of alternative pathways that allow the virus to replicate despite the presence of the drug.
4. Increased efflux of the drug from the virus-infected cell, reducing its intracellular concentration and effectiveness.

Viral drug resistance is a significant concern in the treatment of viral infections such as HIV, hepatitis B and C, herpes simplex virus, and influenza. It can lead to reduced treatment efficacy, increased risk of treatment failure, and the need for more toxic or expensive drugs. Therefore, it is essential to monitor viral drug resistance during treatment and adjust therapy accordingly to ensure optimal outcomes.

Cell fusion is the process by which two or more cells combine to form a single cell with a single nucleus, containing the genetic material from all of the original cells. This can occur naturally in certain biological processes, such as fertilization (when a sperm and egg cell fuse to form a zygote), muscle development (where multiple muscle precursor cells fuse together to create multinucleated muscle fibers), and during the formation of bone (where osteoclasts, the cells responsible for breaking down bone tissue, are multinucleated).

Cell fusion can also be induced artificially in laboratory settings through various methods, including chemical treatments, electrical stimulation, or viral vectors. Induced cell fusion is often used in research to create hybrid cells with unique properties, such as cybrid cells (cytoplasmic hybrids) and heterokaryons (nuclear hybrids). These hybrid cells can help scientists study various aspects of cell biology, genetics, and disease mechanisms.

In summary, cell fusion is the merging of two or more cells into one, resulting in a single cell with combined genetic material. This process occurs naturally during certain biological processes and can be induced artificially for research purposes.

Anti-HIV agents are a class of medications specifically designed to treat HIV (Human Immunodeficiency Virus) infection. These drugs work by interfering with various stages of the HIV replication cycle, preventing the virus from infecting and killing CD4+ T cells, which are crucial for maintaining a healthy immune system.

There are several classes of anti-HIV agents, including:

1. Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs): These drugs act as faulty building blocks that the virus incorporates into its genetic material, causing the replication process to halt. Examples include zidovudine (AZT), lamivudine (3TC), and tenofovir.
2. Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs): These medications bind directly to the reverse transcriptase enzyme, altering its shape and preventing it from functioning properly. Examples include efavirenz, nevirapine, and rilpivirine.
3. Protease Inhibitors (PIs): These drugs target the protease enzyme, which is responsible for cleaving viral polyproteins into functional components. By inhibiting this enzyme, PIs prevent the formation of mature, infectious virus particles. Examples include atazanavir, darunavir, and lopinavir.
4. Integrase Strand Transfer Inhibitors (INSTIs): These medications block the integrase enzyme, which is responsible for inserting the viral genetic material into the host cell's DNA. By inhibiting this step, INSTIs prevent the virus from establishing a permanent infection within the host cell. Examples include raltegravir, dolutegravir, and bictegravir.
5. Fusion/Entry Inhibitors: These drugs target different steps of the viral entry process, preventing HIV from infecting CD4+ T cells. Examples include enfuvirtide (T-20), maraviroc, and ibalizumab.
6. Post-Attachment Inhibitors: This class of medications prevents the virus from attaching to the host cell's receptors, thereby inhibiting infection. Currently, there is only one approved post-attachment inhibitor, fostemsavir.

Combination therapy using multiple classes of antiretroviral drugs has been shown to effectively suppress viral replication and improve clinical outcomes in people living with HIV. Regular adherence to the prescribed treatment regimen is crucial for maintaining an undetectable viral load and reducing the risk of transmission.

"Drug design" is the process of creating and developing a new medication or therapeutic agent to treat or prevent a specific disease or condition. It involves identifying potential targets within the body, such as proteins or enzymes that are involved in the disease process, and then designing small molecules or biologics that can interact with these targets to produce a desired effect.

The drug design process typically involves several stages, including:

1. Target identification: Researchers identify a specific molecular target that is involved in the disease process.
2. Lead identification: Using computational methods and high-throughput screening techniques, researchers identify small molecules or biologics that can interact with the target.
3. Lead optimization: Researchers modify the chemical structure of the lead compound to improve its ability to interact with the target, as well as its safety and pharmacokinetic properties.
4. Preclinical testing: The optimized lead compound is tested in vitro (in a test tube or petri dish) and in vivo (in animals) to evaluate its safety and efficacy.
5. Clinical trials: If the preclinical testing is successful, the drug moves on to clinical trials in humans to further evaluate its safety and efficacy.

The ultimate goal of drug design is to create a new medication that is safe, effective, and can be used to improve the lives of patients with a specific disease or condition.

Peptides are short chains of amino acid residues linked by covalent bonds, known as peptide bonds. They are formed when two or more amino acids are joined together through a condensation reaction, which results in the elimination of a water molecule and the formation of an amide bond between the carboxyl group of one amino acid and the amino group of another.

Peptides can vary in length from two to about fifty amino acids, and they are often classified based on their size. For example, dipeptides contain two amino acids, tripeptides contain three, and so on. Oligopeptides typically contain up to ten amino acids, while polypeptides can contain dozens or even hundreds of amino acids.

Peptides play many important roles in the body, including serving as hormones, neurotransmitters, enzymes, and antibiotics. They are also used in medical research and therapeutic applications, such as drug delivery and tissue engineering.

Secondary protein structure refers to the local spatial arrangement of amino acid chains in a protein, typically described as regular repeating patterns held together by hydrogen bonds. The two most common types of secondary structures are the alpha-helix (α-helix) and the beta-pleated sheet (β-sheet). In an α-helix, the polypeptide chain twists around itself in a helical shape, with each backbone atom forming a hydrogen bond with the fourth amino acid residue along the chain. This forms a rigid rod-like structure that is resistant to bending or twisting forces. In β-sheets, adjacent segments of the polypeptide chain run parallel or antiparallel to each other and are connected by hydrogen bonds, forming a pleated sheet-like arrangement. These secondary structures provide the foundation for the formation of tertiary and quaternary protein structures, which determine the overall three-dimensional shape and function of the protein.

HIV (Human Immunodeficiency Virus) is a species of lentivirus (a subgroup of retrovirus) that causes HIV infection and over time, HIV infection can lead to AIDS (Acquired Immunodeficiency Syndrome). This virus attacks the immune system, specifically the CD4 cells, also known as T cells, which are a type of white blood cell that helps coordinate the body's immune response. As HIV destroys these cells, the body becomes more vulnerable to other infections and diseases. It is primarily spread through bodily fluids like blood, semen, vaginal fluids, and breast milk.

It's important to note that while there is no cure for HIV, with proper medical care, HIV can be controlled. Treatment for HIV is called antiretroviral therapy (ART). If taken as prescribed, this medicine reduces the amount of HIV in the body to a very low level, which keeps the immune system working and prevents illness. This treatment also greatly reduces the risk of transmission.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Viral fusion proteins are specialized surface proteins found on the envelope of enveloped viruses. These proteins play a crucial role in the viral infection process by mediating the fusion of the viral membrane with the target cell membrane, allowing the viral genetic material to enter the host cell and initiate replication.

The fusion protein is often synthesized as an inactive precursor, which undergoes a series of conformational changes upon interaction with specific receptors on the host cell surface. This results in the exposure of hydrophobic fusion peptides or domains that insert into the target cell membrane, bringing the two membranes into close proximity and facilitating their merger.

A well-known example of a viral fusion protein is the gp120/gp41 complex found on the Human Immunodeficiency Virus (HIV). The gp120 subunit binds to CD4 receptors and chemokine coreceptors on the host cell surface, triggering conformational changes in the gp41 subunit that expose the fusion peptide and enable membrane fusion. Understanding the structure and function of viral fusion proteins is important for developing antiviral strategies and vaccines.

Recombinant fusion proteins are artificially created biomolecules that combine the functional domains or properties of two or more different proteins into a single protein entity. They are generated through recombinant DNA technology, where the genes encoding the desired protein domains are linked together and expressed as a single, chimeric gene in a host organism, such as bacteria, yeast, or mammalian cells.

The resulting fusion protein retains the functional properties of its individual constituent proteins, allowing for novel applications in research, diagnostics, and therapeutics. For instance, recombinant fusion proteins can be designed to enhance protein stability, solubility, or immunogenicity, making them valuable tools for studying protein-protein interactions, developing targeted therapies, or generating vaccines against infectious diseases or cancer.

Examples of recombinant fusion proteins include:

1. Etaglunatide (ABT-523): A soluble Fc fusion protein that combines the heavy chain fragment crystallizable region (Fc) of an immunoglobulin with the extracellular domain of the human interleukin-6 receptor (IL-6R). This fusion protein functions as a decoy receptor, neutralizing IL-6 and its downstream signaling pathways in rheumatoid arthritis.
2. Etanercept (Enbrel): A soluble TNF receptor p75 Fc fusion protein that binds to tumor necrosis factor-alpha (TNF-α) and inhibits its proinflammatory activity, making it a valuable therapeutic option for treating autoimmune diseases like rheumatoid arthritis, ankylosing spondylitis, and psoriasis.
3. Abatacept (Orencia): A fusion protein consisting of the extracellular domain of cytotoxic T-lymphocyte antigen 4 (CTLA-4) linked to the Fc region of an immunoglobulin, which downregulates T-cell activation and proliferation in autoimmune diseases like rheumatoid arthritis.
4. Belimumab (Benlysta): A monoclonal antibody that targets B-lymphocyte stimulator (BLyS) protein, preventing its interaction with the B-cell surface receptor and inhibiting B-cell activation in systemic lupus erythematosus (SLE).
5. Romiplostim (Nplate): A fusion protein consisting of a thrombopoietin receptor agonist peptide linked to an immunoglobulin Fc region, which stimulates platelet production in patients with chronic immune thrombocytopenia (ITP).
6. Darbepoetin alfa (Aranesp): A hyperglycosylated erythropoiesis-stimulating protein that functions as a longer-acting form of recombinant human erythropoietin, used to treat anemia in patients with chronic kidney disease or cancer.
7. Palivizumab (Synagis): A monoclonal antibody directed against the F protein of respiratory syncytial virus (RSV), which prevents RSV infection and is administered prophylactically to high-risk infants during the RSV season.
8. Ranibizumab (Lucentis): A recombinant humanized monoclonal antibody fragment that binds and inhibits vascular endothelial growth factor A (VEGF-A), used in the treatment of age-related macular degeneration, diabetic retinopathy, and other ocular disorders.
9. Cetuximab (Erbitux): A chimeric monoclonal antibody that binds to epidermal growth factor receptor (EGFR), used in the treatment of colorectal cancer and head and neck squamous cell carcinoma.
10. Adalimumab (Humira): A fully humanized monoclonal antibody that targets tumor necrosis factor-alpha (TNF-α), used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriasis, and Crohn's disease.
11. Bevacizumab (Avastin): A recombinant humanized monoclonal antibody that binds to VEGF-A, used in the treatment of various cancers, including colorectal, lung, breast, and kidney cancer.
12. Trastuzumab (Herceptin): A humanized monoclonal antibody that targets HER2/neu receptor, used in the treatment of breast cancer.
13. Rituximab (Rituxan): A chimeric monoclonal antibody that binds to CD20 antigen on B cells, used in the treatment of non-Hodgkin's lymphoma and rheumatoid arthritis.
14. Palivizumab (Synagis): A humanized monoclonal antibody that binds to the F protein of respiratory syncytial virus, used in the prevention of respiratory syncytial virus infection in high-risk infants.
15. Infliximab (Remicade): A chimeric monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including Crohn's disease, ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis.
16. Natalizumab (Tysabri): A humanized monoclonal antibody that binds to α4β1 integrin, used in the treatment of multiple sclerosis and Crohn's disease.
17. Adalimumab (Humira): A fully human monoclonal antibody that targets TNF-α, used in the treatment of various inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease, and ulcerative colitis.
18. Golimumab (Simponi): A fully human monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis.
19. Certolizumab pegol (Cimzia): A PEGylated Fab' fragment of a humanized monoclonal antibody that targets TNF-α, used in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease.
20. Ustekinumab (Stelara): A fully human monoclonal antibody that targets IL-12 and IL-23, used in the treatment of psoriasis, psoriatic arthritis, and Crohn's disease.
21. Secukinumab (Cosentyx): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis.
22. Ixekizumab (Taltz): A fully human monoclonal antibody that targets IL-17A, used in the treatment of psoriasis and psoriatic arthritis.
23. Brodalumab (Siliq): A fully human monoclonal antibody that targets IL-17 receptor A, used in the treatment of psoriasis.
24. Sarilumab (Kevzara): A fully human monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis.
25. Tocilizumab (Actemra): A humanized monoclonal antibody that targets the IL-6 receptor, used in the treatment of rheumatoid arthritis, systemic juvenile idiopathic arthritis, polyarticular juvenile idiopathic arthritis, giant cell arteritis, and chimeric antigen receptor T-cell-induced cytokine release syndrome.
26. Siltuximab (Sylvant): A chimeric monoclonal antibody that targets IL-6, used in the treatment of multicentric Castleman disease.
27. Satralizumab (Enspryng): A humanized monoclonal antibody that targets IL-6 receptor alpha, used in the treatment of neuromyelitis optica spectrum disorder.
28. Sirukumab (Plivensia): A human monoclonal antibody that targets IL-6, used in the treatment

... construction and characterization of the first anti-HIV drug delivery system that is triggered to release its contents in the ... HIV Fusion Inhibitors / chemistry* * HIV Fusion Inhibitors / metabolism * HIV Fusion Inhibitors / pharmacokinetics ... Enzymatic triggered release of an HIV-1 entry inhibitor from prostate specific antigen degradable microparticles Int J Pharm. ... and were loaded with the HIV-1 entry inhibitor sodium poly(styrene-4-sulfonate) (pSS). The particles were composed of N-2- ...

https://pubmed.ncbi.nlm.nih.gov/21511017/

... Venanzi Rullo E;Ceccarelli M;Condorelli F; ... Among all the molecules that at present are under investigation, entry and fusion inhibitors pose an interesting class owing to ... Among all the molecules that at present are under investigation, entry and fusion inhibitors pose an interesting class owing to ... and conference communications about all the drugs under investigation belonging to the class of entry and fusion inhibitors ...

https://iris.unikore.it/handle/11387/159425

"HIV Fusion Inhibitors (definition)". www.reference.md. "Qadirvirtide - CTD". ctdbase.org. Qadir, Muhammad Imran (2011). " ... A Perspective for Resistance to HIV Fusion Inhibitors". AIDS Research and Human Retroviruses. 27 (1): 57-63. doi:10.1089/aid. ... These are fusion inhibitors that may be used as prophylaxis or for the treatment of AIDS. These are synthetic peptides composed ... QadirVID-19: He designed a fusion inhibitor for specific treatment of COVID-19, which was named as QadirVID-19. This drug is a ...

https://en.wikipedia.org/wiki/Muhammad_Imran_Qadir

HR212 inhibits HIV-1 access by blocking cell-cell fusion The fusion. HR212 inhibits HIV-1 access by blocking cell-cell fusion ... The fusion between HIV-infected and uninfected cells is the critical step of HIV entry into new target cells. binding of the ... gp41 subunit which subsequently causes membrane fusion. To identify the role of HR212 in the inhibition of HIV-1 entry the ... The result was examined by us of HR212 on the forming of the 6-HB fusion complex by N-PAGE analysis. The peptides moved in the ...

http://www.biosemiotics2013.org/hr212-inhibits-hiv-1-access-by-blocking-cell-cell-fusion-the-fusion/

They do not cure HIV, but fight the infection. Learn more about these medicines. ... There are several different types of HIV medicines. ... Fusion inhibitors block HIV from entering the cells. *CCR5 ... Protease inhibitors (PIs) block an enzyme called protease. Some types of HIV medicines interfere with HIVs ability to infect ... Attachment inhibitors bind to a specific protein on the outer surface of HIV. This prevents HIV from entering the cell. ...

https://medlineplus.gov/hivaidsmedicines.html

Categories: HIV Fusion Inhibitors Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, ...

https://phil.cdc.gov/AdvancedSearchResults.aspx?Search=HIV+Fusion+Inhibitors&parentid=35307&catid=38364

Maraviroc was not antagonistic with the HIV-1 gp41 fusion inhibitor enfuvirtide. Maraviroc was not active against CXCR4-tropic ... with CYP3A Inhibitors) 300 mg Twice Daily (without CYP3A Inhibitors) n Median C min % Subjects with Virologic Success n Median ... Because of the potential for (1) HIV transmission (in HIV-negative infants), (2) developing viral resistance (in HIV-positive ... Instruct women with HIV-1 infection not to breastfeed because HIV-1 can be passed to the baby in breast milk [ see Use in ...

https://www.drugs.com/pro/maraviroc.html

HIV disease is caused by infection with HIV-1 or HIV-2, which are retroviruses in the Retrovir... ... HIV) is a blood-borne virus typically transmitted via sexual intercourse, shared intravenous drug paraphernalia, and mother-to- ... Antiretroviral Agent, Fusion Inhibitor. Class Summary. These agents disrupt the ability of HIV to fuse with and infect healthy ... HIV, Attachment Inhibitors. Class Summary. HIV-1 attachment inhibitors decrease viral replication by binding directly to the ...

http://emedicine.medscape.com/article/211316-medication

Sifuvirtide, a potent HIV fusion inhibitor peptide. Wang RR, Yang LM, Wang YH, Pang W, Tam SC, Tien P, Zheng YT. Biochemical ...

https://www.cheric.org/research/tech/periodicals/searchresult.php?page=100&articlesearch=Wang%20YH&searchtype=author

FUZEON is an HIV-1 gp41 fusion inhibitor indicated for use in combination with other antiretroviral agents for the treatment of ... FUZEON (enfuvirtide) is an inhibitor of the fusion of HIV-1 with CD4 cells. Enfuvirtide is a linear 36-amino acid synthetic ... Because of both the potential for (1) HIV-1 transmission (in HIV-negative infants), (2) developing viral resistance (in HIV- ... Instruct mothers with HIV-1 infection not to breastfeed because HIV-1 can be passed to the baby in breast milk [see Use in ...

https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6935e846-d5a1-49e5-89a2-f8ebe4d5590d

GRFT can inhibit human immunodeficiency virus (HIV) infection at picomolar concentrations, surpassing the ability of most anti- ... HIV agents. The potential to inhibit other viruses as well as parasites has also been demonstrated. Griffithsins antiviral ... is one of the most potent viral entry inhibitors discovered to date. It is currently being developed as a microbicide with ... created a covalently linked fusion protein composed of GRFT and the known HIV entry inhibitor C37 [23]. C37 is a 37-amino acid ...

https://www.mdpi.com/1999-4915/8/10/296

changes leading to fusion, similar to the peptide inhibitors of HIV. fusion. ... The major influenza C virus envelope glycoprotein is called HEF (hemagglutinin-esterase-fusion) because it has the functions of ...

https://virology.ws/2009/09/22/the-a-b-and-c-of-influenza-virus/

Systematic Evaluation of Fluorination as Modification for Peptide-Based Fusion Inhibitors against HIV-1 Infection ... Eine konvergente Totalsynthese des Telomerase-Inhibitors (+-)-gamma-Rubromycin. M. Wilsdorf, H.-U. Reißig, Angew. Chem. 2014, ... Adaptive flexible sialylated nanogels as highly potent influenza A virus inhibitors. Sumati Bhatia, Malte Hilsch, Jose Luis ... Mucin-Inspired, High Molecular Weight Virus Binding Inhibitors Show Biphasic Binding Behavior to Influenza A Viruses ...

https://www.bcp.fu-berlin.de/chemie/chemie/_PaperHighlightsArchive/index.html

Fusion inhibitor: The fusion inhibitor binds to the HIV glycoprotein gp41, alters its structure and prevents the completion of ... Fusion inhibitor: Introduced in 2003, the fusion inhibitor stops the HIV from fusing with the immune cells membrane, ... What is HIV infection?. HIV infection is caused by a virus that infects human immune cells known as T-cells. HIV infection ... Post-attachment inhibitor (Entry inhibitor): The latest ART drug to be approved by FDA in 2018, the post-attachment inhibitor ...

https://hdkino.org/what_art_drugs_prevent_hiv_immune_cell_entry/article.htm

Review this table for Antiretroviral drug use in pregnant women with HIV: pharmacokinetic and toxicity data in pregnancy and ... Entry Inhibitors. Entry and attachment inhibitors block viral binding or fusion of HIV to host cells.. ... If patient has HBV/HIV coinfection, an HBV flare may occur if TDF is stopped; see Hepatitis B Virus/HIV Coinfection. ... nucleoside reverse transcriptase inhibitor; NTD = neural tube defect; NVP = nevirapine; PI = protease inhibitor; PK = ...

https://clinicalinfo.hiv.gov/en/guidelines/perinatal/safety-toxicity-arv-agents-drug-use-pregnant-full

Dimeric C34 Derivatives Linked through Disulfide Bridges as New HIV-1 Fusion Inhibitors, ChemBioChem: Special Issue dedicated ... The concept of multimerised peptides has been applied to HIV-1 envelope proteins related to membrane fusion, hence dimeric C34 ... First OBC Paper: H. Tamamura, T. Kato, A. Otaka & N. Fujii, Synthesis of Potent β-Secretase Inhibitors Containing a ... Thus, in 2003, my first paper with OBC on the development of beta-secretase inhibitors was published1. In addition, we had ...

https://blogs.rsc.org/ob/category/obc-20th-anniversary/?doing_wp_cron=1696079175.8112030029296875000000

The seven major classes of ARVs currently used for HIV treatment are: Fusion Inhibitors (IF), Integrase Inhibitors (II), ... HIV is divided into two types, HIV type 1 (HIV-1) and HIV type 2 (HIV-2). HIV-1 has worldwide distribution, while HIV-2 is more ... Besides, there are also virus-cell inhibitors, which fall into two groups: fusion inhibitors and CCR5 inhibitors. For the use ... and West African mangrove HIV-2 (SIVsm) (5). Thus, it was clear that HIV-1 and HIV-2 were the result of zoonoses from primate- ...

https://www.scielo.sa.cr/scielo.php?script=sci_arttext&pid=S1409-00152020000100101

The fusion inhibitor prevents the membrane of the host CD4 cell from fusing with the HIV envelope. As a result, HIV cannot ... protease inhibitors (PIs), fusion inhibitors, CCR5 antagonists, postattachment inhibitors, integrase strand transfer inhibitors ... Ways HIV can be transmitted. March 4, 2022. www.cdc.gov/hiv/basics/hiv-transmission/ways-people-get-hiv.html. Accessed August 4 ... www.cdc.gov/hiv/basics/statistics.html. Accessed August 4, 2023.. 5. CDC. About HIV/AIDS. June 30, 2022. www.cdc.gov/hiv/basics ...

https://www.uspharmacist.com/article/pioneer-hiv-capsid-inhibitor

HIV fusion inhibitors mechanism of action. A video animation. This animation represents the third step in HIV cell entry: ... Maraviroc (Selzentry, Celsentri), a CCR5 inhibitor for the treatment of HIV infection. An Australian Prescriber review. A ... From Wikipedia Enfuvirtide works by disrupting the HIV-1 molecular machinery at the final stage of fusion with the target cell ... HIV infection Australian Medicines Handbook section 5.4 Highly active antiretroviral therapy has improved survival for patients ...

https://pharmacologycorner.com/tag/ccr5/

Novel strategies in the design of HIV-I fusion/entry inhibitors are based on the construction of dual- targeting fusion ... Peptide Assembly on the Membrane Determines the HIV-1 Inhibitory Activity of Dual-Targeting Fusion Inhibitor Peptides / Gómara ... El envelope proteins from Human Pegivirus with the aim of targeting both the loop region and the fusion peptide domains of HIV- ...

https://ddd.uab.cat/search?f=author&p=Barnadas%20Rodriguez%2C%20Ramon&sc=1&ln=ca

Here we generated a series of lipopeptides derived from EK1 and found that EK1C4 was the most potent fusion inhibitor against ... We previously developed a pan-coronavirus fusion inhibitor, EK1, which targeted the HR1 domain and could inhibit infection by ... protein-mediated cell-cell fusion assay and found that SARS-CoV-2 showed a superior plasma membrane fusion capacity compared to ... EK1C4 was also highly effective against membrane fusion and infection of other human coronavirus pseudoviruses tested, ...

https://www.nature.com/articles/s41422-020-0305-x?error=cookies_not_supported&code=3ca67ab7-7f0a-4c9e-91ee-9fbcf51d0c35

Fusion inhibitors block HIV from entering the (CD4 cells) of the .. My life has changed in a really positive way. Ed Rosen CJ, ... using a combination treatment of aspirin with a P2Y12 platelet inhibitor after percutaneous coronary intervention (PCI), ...

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fusion inhibitor. 融合阻害剤. heat-treated blood products. 加熱血液製剤. ... human immunodeficiency virus ,HIV. HIVウイルス、ヒト免疫欠如症ウイルス. ... 注目の話題から調べる [HIV/エイズ] Last Updated: October 3, 2023. ... non-nucleoside

https://rnnnews.jp/indepth/pg/print?ch=302

New drugs called attachment inhibitors and fusion inhibitors are being tested in humans. ... How Do I Know If I Have HIV?. The only way to know for sure if you have HIV is to get an HIV test. ... The different types of anti-HIV drugs each target a different aspect of HIVs life cycle:. *. Entry. HIV has to get into a T ... Several protease inhibitors (or PIs) are now on the market. Another approach is to make the bodys immune system fight HIV more ...

http://www.health.am/topics/more/hiv_symptoms_aids_hiv_detection_and_treatment/

HIV Fusion Inhibitors MeSH DeCS ID:. 8732 Unique ID:. D008561 NLM Classification:. QU 375 ... Membrane Fusion - Preferred Concept UI. M0013335. Scope note. The adherence and merging of cell membranes, intracellular ...

https://decs.bvsalud.org/en/ths/resource/?id=8732

HIV Fusion Inhibitors. 1. 2007. 2. 0.020. Why? Receptors, CCR5. 1. 2007 ...

https://profiles.musc.edu/display/person/ericgmeissner/network/researchareas/details

HIV Fusion Inhibitors. Date of Entry. 2004/02/13. Revision Date. 2020/02/28. ... Anti-HIV Agents. Registry Number. LT369U66CE. Heading Mapped to. *Antibodies, Monoclonal Frequency. 52. Note. prevents entry of ... human immunodeficiency virus (HIV) into the host cell. TNX-355 binds to the CD4 receptor on the cells surface, an entry gate ...

https://meshb-prev.nlm.nih.gov/record/ui?ui=C481504

Up-to-date information about approved and experimental therapies for HIV/AIDS, Hepatitis, and related conditions. ... HIV Glasgow: Long-Acting HIV Fusion Inhibitor Albuvirtide Regimen Matches Standard Therapy Details. Category: Experimental HIV ... A new fusion inhibitor, albuvirtide, under development in China, combined with a boosted protease inhibitor, proved just as ... New HIV Capsid Inhibitors Show High Potency and Prolonged Activity in Early Studies Details. Category: Experimental HIV Drugs ...

http://w3w.hivandhepatitis.com/hiv-treatment/experimental-hiv-drugs

http://www.vaccineinformation.labtestsonline.hepprograms.niddk.hivandhepatitis.com/hiv-treatment/experimental-hiv-drugs

These outcomes indicate that HR212 will not stop HIV-1 binding to either the principal receptor Compact disc4 or the coreceptors CXCR4 and CCR5. (biosemiotics2013.org)
CCR5 antagonists and post-attachment inhibitors block different molecules on the CD4 cells. (medlineplus.gov)
Maraviroc tablet is a CCR5 co-receptor antagonist indicated in combination with other antiretroviral agents for the treatment of only CCR5-tropic HIV-1 infection in adults and pediatric patients 2 years of age and older weighing at least 10 kg. (drugs.com)
Prior to initiation of maraviroc tablets for treatment of HIV-1 infection, test all patients for CCR5 tropism using a highly sensitive tropism assay. (drugs.com)
Developed in 2007, the chemokine receptor antagonist blocks entry of certain specific strains of HIV, which attach to a particular protein on the immune cell's surface known as chemokine receptor 5 (CCR5). (hdkino.org)
Maraviroc (Selzentry, Celsentri), a CCR5 inhibitor for the treatment of HIV infection. (pharmacologycorner.com)
FDA-approved ARVs are categorized into eight pharmacologic classes, including the nucleoside reverse transcriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), fusion inhibitors, CCR5 antagonists, postattachment inhibitors, integrase strand transfer inhibitors (INSTIs), and now the novel class of capsid inhibitors. (uspharmacist.com)
HIV attaches to the CD4 receptor and binds to coreceptors, CCR5 or CXCR4, which facilitates entry of the virus into the cell. (uspharmacist.com)
CCR5 antagonists prevent CD4 cells from expressing their CCR5 coreceptor, which stops HIV from entering the CD4 cell. (uspharmacist.com)
Postattachment inhibitors bind to the host CD4 receptor and block HIV from binding to the CCR5 and CXCR4 coreceptors. (uspharmacist.com)
Moreover, DPHB selectively inhibited HIV-1 strains that use CXCR4 or both CXCR4 and CCR5 co-receptors for entry, but not strains exclusively using CCR5. (ox.ac.uk)
These in vivo validated inhibitors are the CCR5 antagonists PSC-RANTES and CMPD-167 the gp120-binding small-molecule BMS-806 the gp41 peptide fusion inhibitor C52L as well as the gp120-binding proteins cyanovirin-N (9-11). (sciencepop.org)
Although many naturally sent HIV-1 strains only use CCR5 a little but significant small fraction of new attacks does involve infections that also or rather enter cells via CXCR4 (15 16 Therefore using three problem infections with different coreceptor utilization information allowed us to measure whether an individual microbicide candidate could possibly be protective inside a tropism-independent way. (sciencepop.org)
2012. Sustained release of the CCR5 inhibitors CMPD167 and maraviroc from vaginal rings in rhesus macaques. . (cornell.edu)
2011. Resistance of a human immunodeficiency virus type 1 isolate to a small molecule CCR5 inhibitor can involve sequence changes in both gp120 and gp41. . (cornell.edu)
2010. Protection of rhesus macaques from vaginal infection by vaginally delivered maraviroc, an inhibitor of HIV-1 entry via the CCR5 co-receptor. . (cornell.edu)
2009. Inefficient entry of vicriviroc-resistant HIV-1 via the inhibitor-CCR5 complex at low cell surface CCR5 densities. . (cornell.edu)
2009. Resistance to CCR5 inhibitors caused by sequence changes in the fusion peptide of HIV-1 gp41. . (cornell.edu)
2008. Neutralizing antibody and anti-retroviral drug sensitivities of HIV-1 isolates resistant to small molecule CCR5 inhibitors. . (cornell.edu)
Mouse monoclonal to RUNX1 Because of the multi-step character from the HIV access, you can rationalize that merging a coreceptor inhibitor, like a CCR5 antibody, having a fusion peptide, such as for example enfuvirtide (ENF), into one molecule may be an beneficial method of prevent access of HIV towards the sponsor cells at multiple methods. (bioinbrief.com)
Right here we describe some experiments utilizing a book HIV access inhibitor, comprising a CCR5 antibody that is covalently associated with a fusion peptide inhibitor. (bioinbrief.com)
Maraviroc originally designated as UK-427857 and approved in August 2007 [1] blocks the binding between gp120 and chemokine receptor CCR5 which HIV-1 uses as a coreceptor. (biomasswars.com)

It is the final stage of infection with HIV. (medlineplus.gov)
The medicines do not cure HIV infection, but help people with HIV live longer, healthier lives. (medlineplus.gov)
Effective antiretroviral therapy is the most important intervention in terms of improving longevity and preventing opportunistic infections in patients with human immunodeficiency virus (HIV) infection. (medscape.com)
For more information, see Pediatric HIV Infection . (medscape.com)
FUZEON is an HIV-1 gp41 fusion inhibitor indicated for use in combination with other antiretroviral agents for the treatment of HIV-1 infection in treatment-experienced patients with HIV-1 replication despite ongoing antiretroviral therapy. (nih.gov)
GRFT can inhibit human immunodeficiency virus (HIV) infection at picomolar concentrations, surpassing the ability of most anti-HIV agents. (mdpi.com)
What is antiretroviral therapy (ART) for human immunodeficiency virus (HIV) infection? (hdkino.org)
Antiretroviral therapy (ART) is a complete treatment regimen for human immunodeficiency virus ( HIV ) infection, with a combination of three or more classes of drugs . (hdkino.org)
HIV infection has no cure but ART can contain the viral growth and keep the patient healthy and active for many years. (hdkino.org)
What is HIV infection? (hdkino.org)
HIV infection is caused by a virus that infects human immune cells known as T-cells. (hdkino.org)
HIV infection spreads through certain bodily fluids such as blood, semen, vaginal fluids or breast milk . (hdkino.org)
In its later stages, HIV infection can lead to acquired immune deficiency syndrome ( AIDS ), when the immune system is so weakened that it is unable to fight even common infections. (hdkino.org)
HIV is grouped into the genus Lentivirus (lentus, from Latin) due to the slow course of infection and thus disease, with a long latency period, persistent viral replication and central nervous system involvement ( 1 ). (scielo.sa.cr)
ABSTRACT: Lenacapavir (Sunlenca) is the first FDA-approved drug in the novel class of HIV capsid inhibitors for heavily treatment-experienced adults with multidrug-resistant HIV-1 infection after failing their current antiretroviral regimen. (uspharmacist.com)
Lenacapavir is a novel, first-in-class HIV capsid inhibitor that was FDA approved on December 22, 2022, for heavily treatment-experienced adults with multidrug-resistant HIV-1 infection after failing their current antiretroviral (ARV) regimen due to resistance, intolerance, or safety considerations. (uspharmacist.com)
HIV is an infection that poses significant public health challenges worldwide. (uspharmacist.com)
6 Initial symptoms of HIV infection can resemble flu-like symptoms, including fever, fatigue, sore throat, and swollen lymph nodes. (uspharmacist.com)
HIV infection progresses through three stages: the acute stage, clinical latency stage, and acquired immunodeficiency syndrome (AIDS) stage. (uspharmacist.com)
We previously developed a pan-coronavirus fusion inhibitor, EK1, which targeted the HR1 domain and could inhibit infection by divergent human coronaviruses tested, including SARS-CoV and MERS-CoV. (nature.com)
Here we generated a series of lipopeptides derived from EK1 and found that EK1C4 was the most potent fusion inhibitor against SARS-CoV-2 S protein-mediated membrane fusion and pseudovirus infection with IC50s of 1.3 and 15.8 nM, about 241- and 149-fold more potent than the original EK1 peptide, respectively. (nature.com)
EK1C4 was also highly effective against membrane fusion and infection of other human coronavirus pseudoviruses tested, including SARS-CoV and MERS-CoV, as well as SARSr-CoVs, and potently inhibited the replication of 5 live human coronaviruses examined, including SARS-CoV-2. (nature.com)
Soon after HIV infection, the body begins to make antibodies that fight the virus. (health.am)
If you know you are at high risk of HIV infection and come down with a bad case of the flu , see a doctor right away. (health.am)
It could be the early signs of HIV infection. (health.am)
There are very sensitive tests that can tell if you've got HIV - and treatment during this very early stage of infection works best. (health.am)
HIV infection isn't a death sentence. (health.am)
Everybody agrees that starting aggressive treatment in the early days after infection - the stage of acute HIV infection - is most effective. (health.am)
But most people don't find out they have HIV until the stage of chronic HIV infection, when the virus has a firm hold on the body. (health.am)
A new fusion inhibitor, albuvirtide, under development in China, combined with a boosted protease inhibitor, proved just as effective as a triple regimen of lopinavir/ritonavir plus 2 NRTIs for treatment-experienced HIV patients, according to a report at the International Congress on Drug Therapy in HIV Infection last month in Glasgow. (hivandhepatitis.com)
Acquired immunodeficiency syndrome (AIDS) is the most advanced stage of infection with HIV. (rxwiki.com)
The first signs of HIV infection may be swollen glands and flu-like symptoms. (rxwiki.com)
The symptoms of HIV infection and AIDS vary, depending on the phase of infection. (rxwiki.com)
Symptoms related to acute HIV infection (when a person is first infected) are often flu-like. (rxwiki.com)
Acute HIV infection progresses over a few weeks to months to become an asymptomatic (no symptoms) HIV infection. (rxwiki.com)
Human Immunodeficiency Virus (HIV) Infection Human immunodeficiency virus (HIV) infection is a viral infection that progressively destroys certain white blood cells and is treated with antiretroviral medications. (msdmanuals.com)
Several classes of antiretroviral medications are used together to treat HIV infection. (msdmanuals.com)
These are used mainly for HIV infection that is resistant to several other medications. (msdmanuals.com)
Medications used to treat HIV infection were developed based on the life cycle of HIV. (msdmanuals.com)
microbicides remain a potential way to protect females against an infection by HIV type 1 1351635-67-0 supplier (HIV-1) during sexual activity (1-3). (sciencepop.org)
Many inhibitors of HIV-1 fusion with cells have already been shown to defend macaques from an infection using a simian/individual immunodeficiency trojan (SHIV) after genital application a short while before problem via the same path. (sciencepop.org)
We utilized three different problem infections SHIV-162P3 SHIV-89.6P and SHIV-KU1 allowing all of us to create some assessment from the breadth of activity of T-1249 against divergent strains and more significantly to determine whether an individual inhibitor could drive back viruses that use different coreceptors for infection. (sciencepop.org)
The war on HIV infection wages as fiercely as ever, but if research into a class of drugs known as a fusion inhibitors turns out to be as promising as results presented this month to an international AIDS conference in Buenos Aires suggest, clinicians may soon have a powerful new addition to their armamentarium. (the-scientist.com)
This inhibition reduces viral replication, hence progression form HIV infection to. (the-scientist.com)
2012. Env-glycoprotein heterogeneity as a source of apparent synergy and enhanced cooperativity in inhibition of HIV-1 infection by neutralizing antibodies and entry inhibitors. . (cornell.edu)
The number of cases of human immunodeficiency virus (HIV) infection among young adolescents had been increasing over the years. (medscape.com)
CDC estimates that 21% of the approximately 36,801 people newly diagnosed with HIV infection in 2019 were aged 13-24 years. (medscape.com)
In contrast, perinatal HIV infection is relatively rare in the United States, and most perinatally infected youth are now older and aging out of pediatric care, setting the stage for an increased need for transitional care. (medscape.com)
therefore, dosage of medications for HIV infection should be based on the SMR (also known as Tanner staging) of puberty and not just on age alone. (medscape.com)
HIV-1 fusion/entry inhibitors unlike most clinical anti-HIV drugs that act after infection occurs not only intercept the virus before it invades the target cell but also can be used as prophylactic agents to assemble a barrier against the initial infection. (biomasswars.com)
Enfuvirtide a peptide originally designated as T20 and approved in April 2003 [2] is the first fusion inhibitor used in combination therapy for the treatment of Sulbactam HIV-1 infection. (biomasswars.com)
This report modifies and expands the list of antiretroviral human immunodeficiency virus (HIV) infection, appropri- medications that can be considered for use as PEP. (cdc.gov)
Increasing risk factors for leishmaniasis include urbanization, extended agricul- tural projects and civil unrest and the increase in patients with Leishmania infantum and HIV co-infection in the Region may signal a new threat. (who.int)

Although data from cohorts in the United States have not shown an increased risk of preterm birth with combination therapy, a European collaborative study showed an increased risk of preterm labor in women infected with HIV who were taking combination antiretroviral therapy, with an odds ratio for preterm birth of 1.8 for combination therapy without a protease inhibitor and 2.6 for combination therapy that included a protease inhibitor. (medscape.com)

From Wikipedia Enfuvirtide works by disrupting the HIV-1 molecular machinery at the final stage of fusion with the target cell, preventing uninfected cells from becoming infected. (pharmacologycorner.com)
There is so far only one fusion inhibitor for HIV treatment which is enfuvirtide . (expasy.org)
Enfuvirtide treatment remains complicated since it is the only anti-HIV compound that is not orally available. (expasy.org)
Example: Fusion inhibitors such as enfuvirtide target HIV by binding to the gp41 protein involved in membrane fusion. (researchpeptides.net)

Long-acting injectable contraception is compatible with protease inhibitors and NNRTIs, but data are limited with integrase inhibitors. (medscape.com)

To identify the role of HR212 in the inhibition of HIV-1 entry the following experiments were performed. (biosemiotics2013.org)
NRTIs interfere with HIV reverse transcriptase by competitive inhibition. (hiv.gov)
However, it was found that pure DPHB was not active against HIV-1 and that its degradation products (most likely polyanions) were responsible for inhibition of viral fusion. (ox.ac.uk)
1. Inhibition of viral fusion: Peptides can interfere with the fusion process between viral membranes and host cell membranes, preventing viral entry into host cells. (researchpeptides.net)
Furthermore, this process allowed us to 3544-24-9 IC50 explore the synergy of inhibition of HIV access. (bioinbrief.com)
Small molecule inhibition of HIV fusion continues to be an elusive goal despite many years of effort by both pharmaceutical and educational laboratories. (biomasswars.com)
Additionally a book site for little molecule inhibition of fusion has been suggested regarding residues of the loop and fusion peptide. (biomasswars.com)
Despite the challenges there are significant advantages to small molecule inhibition of fusion including the potential for low cost and oral bioavailability simpler formulation and the ability to overcome. (biomasswars.com)

Maraviroc tablets are contraindicated in patients with severe renal impairment or end-stage renal disease (ESRD) (CrCl less than 30 mL per minute) who are concomitantly taking potent CYP3A inhibitors or inducers. (drugs.com)
Griffithsin (GRFT), an algae-derived lectin, is one of the most potent viral entry inhibitors discovered to date. (mdpi.com)
A novel type of antiretroviral drug that interferes with the assembly and disassembly of the HIV capsid, which encloses the genetic blueprint of the virus, may offer a new potent and long-acting treatment option if it continues to look promising in larger studies, according to a presentation at the Conference on Retroviruses and Opportunistic Infections this month in Seattle. (hivandhepatitis.com)
Bictegravir, an investigational integrase inhibitor from Gilead Sciences, was highly potent, well tolerated and worked as well as dolutegravir (Tivcay) in a Phase 2 clinical trial, according to study results presented at the 2017 Conference on Retroviruses and Opportunistic Infections (CROI) this week in Seattle and published online in The Lancet HIV . (hivandhepatitis.com)
BMS-378806 a much less potent substance in the same inhibitor course shielded macaques from SHIV-162P3 genital challenge. (sciencepop.org)

The latest ART drug to be approved by FDA in 2018, the post-attachment inhibitor prevents the viral envelope fusion with the cell membrane after it binds to the cell. (hdkino.org)
Post-attachment inhibitors also prevent HIV from entering cells but in a different way from fusion inhibitors. (msdmanuals.com)
The overall classes of medications that act against HIV at this stage are called entry inhibitors, and they included attachment inhibitors, post-attachment inhibitors, and fusion inhibitors. (msdmanuals.com)
A post attachment step consists in the fusion of viral and host membranes. (expasy.org)

The loss of these cells makes it hard for your body to fight off infections and certain HIV-related cancers. (medlineplus.gov)
Even though there is still some HIV in your body, your immune system should be strong enough to fight off infections and certain HIV-related cancers. (medlineplus.gov)
HIV attacks the body's immune system by targeting CD4 T-cells, which are essential to fight off infections and diseases. (uspharmacist.com)
If not treated, HIV gradually weakens the immune system, leading to opportunistic infections and other serious illnesses. (uspharmacist.com)
A pair of long-acting monoclonal antibodies that prevent HIV from entering human cells -- ibalizumab and PRO 140 -- may offer new treatment options for people with highly resistant virus and limited treatment options, researchers reported at the Conference on Retroviruses and Opportunistic Infections (CROI) last week in Seattle. (hivandhepatitis.com)
People with AIDS have had their immune system damaged by HIV, and they are at very high risk of getting infections that are uncommon in people with a healthy immune system. (rxwiki.com)
Furthermore T-1249 was broadly and potently energetic in vitro against disease of PBMCs with a -panel of HIV-1 isolates from multiple hereditary subtypes and it inhibited multiple HIV-1 Env-pseudotyped infections from clinical examples with IC50 ideals ≈10 nM. (sciencepop.org)
67% of all people living with HIV worldwide live in sub-Saharan Africa, and 91% of all new infections among children occur there. (medscape.com)
improved pharmacokinetic guidelines for any fusion inhibitor in human beings and the mix of two dynamic antiviral agents in a single molecule might provide better toughness in managing the introduction of resistant infections. (bioinbrief.com)
Introduction Enveloped infections, such as for example HIV-1, use membrane destined fusion proteins to mediate connection and access into specific focus on sponsor cells. (bioinbrief.com)
It's been more developed that R5-tropic infections are nearly specifically present through the severe illness with HIV-1 as well as the asymptomatic stage, whereas X4-tropic infections emerge in later on stages of HIV illness and are related to a far more dramatic Compact disc4 cell decrease and development towards Helps [5,6]. (bioinbrief.com)
The Centers for Disease Control and Prevention (CDC) data spanning 2015-2019 demonstrate a 15% decrease in HIV infections in the 13-24 year old age group. (medscape.com)
Introduction The arrival of numerous antiretroviral drugs offers resulted in a decrease in AIDS-related deaths but has not reduced the number of people living Igf2 with Human being Immunodeficiency Disease Type 1 (HIV-1) illness or significantly affected the number of fresh infections annually. (biomasswars.com)

2009. Addition of a cholesterol group to an HIV-1 peptide fusion inhibitor dramatically increases its antiviral potency. . (cornell.edu)

If patients with severe renal impairment or ESRD receiving maraviroc (without concomitant CYP3A inducers or inhibitors) experience postural hypotension, the dose of maraviroc should be reduced from 300 mg twice daily to 150 mg twice daily. (drugs.com)

Novel strategies in the design of HIV-I fusion/entry inhibitors are based on the construction of dual- targeting fusion proteins and peptides with synergistic antiviral effects. (uab.cat)
HIV-1 entry and fusion with target cells is an important target for antiviral therapy. (ox.ac.uk)
Outcomes Antiviral activity of the bifunctional HIV-entry inhibitor The brief plasma half-life of ENF needs twice daily shots [17], this dosing hassle offers markedly limited the broader usage of ENF. (bioinbrief.com)
A lot of antiviral peptides have already been created against HIV fusion (for review discover [7] in addition to Cai et al in this problem) but little molecule drug advancement has proved especially challenging for several reasons. (biomasswars.com)

In this work we describe the design of dual -targeting peptides composed of peptide domains of E2 and El envelope proteins from Human Pegivirus with the aim of targeting both the loop region and the fusion peptide domains of HIV-I gp41. (uab.cat)

Attachment inhibitors bind to a specific protein on the outer surface of HIV. (medlineplus.gov)

Reverse transcriptase inhibitors prevent HIV reverse transcriptase from converting HIV RNA into DNA. (msdmanuals.com)
These medications prevent HIV entry into its target cells or inhibit the three enzymes (reverse transcriptase, integrase, and protease) that the virus uses to replicate. (msdmanuals.com)
The first clinical description of HIV resistance to an antiretroviral agent was published in 1989, when patients taking zidovudine monotherapy accumulated mutations within the reverse transcriptase gene, resulting in a marked increase in drug resistance [ 1 ]. (medilib.ir)
Genotypic resistance assays detect the presence of specific drug resistance mutations in the regions of the HIV genome encoding protease, reverse transcriptase, and integrase. (medilib.ir)

It interferes with HIV capsid assembly, virus assembly and release, and nuclear transport. (uspharmacist.com)

There's been great fascination with discovering little molecule alternatives as inhibitors focusing on gp41 within the last 10 years. (biomasswars.com)

These are fusion inhibitors that may be used as prophylaxis or for the treatment of AIDS. (wikipedia.org)
Without treatment, HIV can gradually destroy the immune system and advance to AIDS. (medlineplus.gov)
Not everyone with HIV develops AIDS. (medlineplus.gov)
The need for the study of microbiological expertise can be applied in biocrimes linked to the transmission of microorganisms intentionally, such as the intentional transmission of Human Immunodeficiency Virus (HIV), a pathogen that causes Acquired Immunodeficiency Syndrome (AIDS). (scielo.sa.cr)
The position of the United Nations Joint Program on HIV / AIDS, to avoid further discrimination against carriers, is to avoid establishing legislation to address the issue or a specific criminal type. (scielo.sa.cr)
The first clue to the emergence of HIV-2 came in 1986 when a morphologically similar but previously distinct virus was found to cause AIDS in patients in West Africa ( 4 ). (scielo.sa.cr)
Uncontrolled HIV can progress to AIDS. (uspharmacist.com)
Treatment with combinations of AIDS drugs can keep people with HIV from getting AIDS. (health.am)
Most AIDS/HIV doctors now recommend holding off on treatment until a person's immune system starts to fail. (health.am)
Acquired immunodeficiency syndrome (AIDS) is a chronic, potentially life-threatening condition caused by HIV. (rxwiki.com)
HIV will eventually progress and weakens your immune system to the point that you have AIDS. (rxwiki.com)
There is no cure for HIV/AIDS, but there are medications that can dramatically slow the progression of the disease and people with HIV can live longer, healthier lives than in the past. (rxwiki.com)
If not treated, almost all people infected with HIV will develop AIDS. (rxwiki.com)
Early in the acquired immunodeficiency syndrome (AIDS) epidemic, women were rarely diagnosed with HIV or AIDS, but by 2005, women represented 27% of the estimated 45,669 new diagnosis of HIV/AIDS, with the greatest rise among young women. (medscape.com)
Furthermore, women of color account for 80% of newly diagnosed HIV/AIDS cases. (medscape.com)
As HIV continues to develop resistance to the present antiretrovirals a new class of drugs offer hope for the treatment of AIDS. (the-scientist.com)
There may also be signs and symptoms of infectious disease related to HIV/AIDS or hepatitis. (medscape.com)

Microgel particles were synthesized with a crosslinker containing a peptide substrate for the seminal serine protease prostate specific antigen (PSA) and were loaded with the HIV-1 entry inhibitor sodium poly(styrene-4-sulfonate) (pSS). (nih.gov)
These block the entry of HIV genome into human CD4 cells by binding to HR1 region of spike protein of HIV, so that the virus can not come close to the human cell membrane and ultimately fusion of the viral envelope with human cell membrane is prevented. (wikipedia.org)
HR212 inhibits HIV-1 access by blocking cell-cell fusion The fusion between HIV-infected and uninfected cells is the critical step of HIV entry into new target cells. (biosemiotics2013.org)
What ART Drugs Prevent HIV Entry into the Human Immune Cell? (hdkino.org)
What ART drug classes prevent entry of human immunodeficiency virus (HIV) into the human immune cell? (hdkino.org)
Introduced in 2003, the fusion inhibitor stops the HIV from fusing with the immune cell's membrane, preventing entry. (hdkino.org)
This animation represents the third step in HIV cell entry: fusion. (pharmacologycorner.com)
The first step in the HIV life cycle is attachment and entry. (uspharmacist.com)
This consideration has fueled efforts to develop new bioavailable inhibitors targeting different steps of the HIV-1 entry process. (ox.ac.uk)
Here, a high-throughput screen was performed of a large library of 100,000 small molecules for HIV-1 entry/fusion inhibitors, using a direct virus-cell fusion assay in a 384 half-well format. (ox.ac.uk)
prevents entry of human immunodeficiency virus ( HIV ) into the host cell. (nih.gov)
Entry (fusion) inhibitors prevent HIV from entering cells. (msdmanuals.com)
One type of entry inhibitor, CCR-5 inhibitors, blocks the CCR-5 receptor, preventing HIV from entering human cells. (msdmanuals.com)
For newly diagnosed patients, the U.S. Department of Health and Human Services recommends testing for HIV drug resistance at entry into care. (managedhealthcareexecutive.com)
2007. Entry inhibitor-based microbicides are active in vitro against HIV-1 isolates from multiple genetic subtypes. . (cornell.edu)

The HIV test looks for these antibodies in your blood. (health.am)
After about three months, most people have enough anti-HIV antibodies to test positive on standard HIV tests. (health.am)
2018. Epitopes for neutralizing antibodies induced by HIV-1 envelope glycoprotein BG505 SOSIP trimers in rabbits and macaques. . (cornell.edu)
HIV-1 neutralizing antibodies induced by native-like envelope trimers. (cornell.edu)

4. With the help of an enzyme called integrase (also produced by HIV), the viral DNA becomes integrated with the cell's DNA. (msdmanuals.com)

The major influenza C virus envelope glycoprotein is called HEF (hemagglutinin-esterase-fusion) because it has the functions of both the HA and the NA. (virology.ws)
2019. Closing and Opening Holes in the Glycan Shield of HIV-1 Envelope Glycoprotein SOSIP Trimers Can Redirect the Neutralizing Antibody Response to the Newly Unmasked Epitopes. . (cornell.edu)
2018. cGMP production and analysis of BG505 SOSIP.664, an extensively glycosylated, trimeric HIV-1 envelope glycoprotein vaccine candidate. . (cornell.edu)

This interaction leads to the formation of the fusion-active 6-HB of the buy Bedaquiline (TMC-207) gp41 subunit which subsequently causes membrane fusion. (biosemiotics2013.org)
HR212 blocks gp41 6-HB development The conformational modification of gp41 to create the 6-HB framework is crucial for membrane fusion of HIV-1 with focus on cells. (biosemiotics2013.org)
Therefore, we herein established a SARS-CoV-2 spike (S) protein-mediated cell-cell fusion assay and found that SARS-CoV-2 showed a superior plasma membrane fusion capacity compared to that of SARS-CoV. (nature.com)

Functional experiments revealed that DPHB caused irreversible inactivation of HIV-1 Env on cell-free virions and that this effect was related to binding to the third variable loop (V3) of the gp120 subunit of HIV-1 Env. (ox.ac.uk)
2009. Enzymatic removal of mannose moieties can increase the immune response to HIV-1 gp120 in vivo. . (cornell.edu)

In another review Sulbactam in this problem the protective aftereffect of a jeopardized gp41 fusion system on bystander T-cell disease is discussed. (biomasswars.com)

Subsequently, HIV variants resistant to every available antiretroviral agent have been identified. (medilib.ir)

TNF Alpha Inhibitors Market Overview 2023-2032 - Market Growth Analysis, Trends And Drivers - TNF alpha inhibitors refer to medications that are used to treat inflammatory diseases such as rheumatoid arthritis (RA), psoriatic arthritis, and juvenile idiopathic arthritis and that help to reduce or eliminate inflammation. (powershow.com)
TNF Alpha Inhibitors Market Future Demand And Leading Players Forecast To 2023 - A recent report published by The Business Research Company on TNF Alpha Inhibitors Global Market provides in-depth analysis of segments and sub-segments in the global as well as regional. (powershow.com)

Its unique resistance profile offers promise for patients with multidrug-resistant HIV. (uspharmacist.com)
10 From 2000 to 2009, 14% of ART-naive patients with HIV had drug resistance mutations to at least one drug class, 2% had mutations with resistance for two or more classes, and less than 1% had mutations for triple-class resistance. (managedhealthcareexecutive.com)
11 In an observational study from 2000 to 2006, 8% of patients with HIV who received prior ART therapy displayed triple-class resistance, with an overall incidence rate of 13 triple-class resistant cases per 1,000 person-years of ART exposure. (managedhealthcareexecutive.com)
12 Thankfully, successful use of combined ART and improved treatment options have resulted in the decline of HIV drug resistance. (managedhealthcareexecutive.com)
HIV drug-resistance testing is also recommended in patients changing ART regimens who have virologic failure and HIV-RNA levels greater than 200 copies/mL, and in those with suboptimal viral load reduction. (managedhealthcareexecutive.com)
Drug-induced and transmitted resistance remains a concern with existing antiretroviral options for the management of HIV, 20 especially as MDR HIV is associated with an increase in mortality. (managedhealthcareexecutive.com)
INTRODUCTION - The use of drug resistance testing has become an integral part of HIV clinical care. (medilib.ir)
This topic will provide an overview of HIV drug resistance testing. (medilib.ir)
See "Interpretation of HIV drug resistance testing" and "Selecting an antiretroviral regimen for treatment-experienced patients with HIV who are failing therapy" and "Evaluation of the treatment-experienced patient failing HIV therapy" . (medilib.ir)
As an example, in an observational study of more than 2699 HIV-infected patients who were eligible for genotypic and phenotypic testing between 1999 and 2005, resistance testing was associated with improved survival (adjusted hazard ratio, 0.69 [95% CI 0.51-0.94]) after controlling for demographics, CD4 cell count, HIV RNA level, and intensity of clinical follow-up [ 3 ]. (medilib.ir)
See "Interpretation of HIV drug resistance testing" . (medilib.ir)
As an example, some mutations cause resistance to certain drugs but increase susceptibility to others, while other mutations may impact viral fitness (see "Interpretation of HIV drug resistance testing", section on 'Viral fitness' ). (medilib.ir)
HIV has developed resistance to existing therapies (protease inhibitors and reverse transcription inhibitors) and, secondly, drug companies and regulators have halted a number of early stage clinical trials because of adverse effects. (the-scientist.com)
Many of these young adults are very treatment-experienced and can harbor significant HIV resistance mutations and comorbidities associated with past treatment. (medscape.com)

These medications block HIV from entering human cells or block the activity of one of the enzymes HIV needs to replicate inside human cells and/or integrate its genetic material into human DNA. (msdmanuals.com)
At this stage, medications called integrase inhibitors can prevent HIV DNA from being integrated into human DNA. (msdmanuals.com)
At this stage, medications called protease inhibitors can prevent the maturation of the HIV virus. (msdmanuals.com)
HIV PEP regimens and other medications, consultation with these recommendations have been updated twice ( 1-3 ). (cdc.gov)

The human immunodeficiency virus (HIV) kills or damages the body's immune system. (rxwiki.com)
By damaging your immune system, HIV interferes with your body's ability to fight the organisms that cause disease. (rxwiki.com)
Whilst the detail is complex, the principal underlying fusion inhibitors is straightforward: they inhibit the fusion of HIV with receptors on the surface of the immune system cells - CD4+, a subset of T-lymphocytes - that HIV interacts with prior to infecting the cells. (the-scientist.com)

3 In the United States alone, approximately 1.2 million people are living with HIV, with nearly 37,800 new cases reported in 2019. (uspharmacist.com)
13-15 In 2019, nearly 1.2 million people at least 13 years of age were living with HIV in the United States. (managedhealthcareexecutive.com)

Fig. 1: Establishment of SARS-CoV-2 S protein-mediated cell-cell fusion system. (nature.com)
The data points to the need for a strongly amphiphilic character of the inhibitors probably as a means to mediate the membrane - protein interaction that occurs in gp41 in addition to the protein - protein connection that accompanies the fusion-activating conformational transition. (biomasswars.com)

Globally, the CDC estimates that there are 38 million people living with HIV as of 2020. (uspharmacist.com)

CXCR4 is one of several chemokine receptors that HIV can use to infect CD4+ T cells . (wikidoc.org)

To enter a human cell, HIV must bind to a CD4 receptor and one other receptor, such as the CCR-5 receptor. (msdmanuals.com)
The decision from the co-receptor mixed up in fusion process offers provided rise to this is of viral tropism. (bioinbrief.com)
So that they can enhance the em in vivo /em pharmacokinetic properties a prototypic recombinant antibody-FI fusion proteins was generated, where two T-2635 fusion inhibitors had been covalently from the C-terminal ends of both heavy chains of the monoclonal antibody against the insulin-like development factor-I receptor (IGF-IR). (bioinbrief.com)
Inhibitors against gp41 possess the capacity Sulbactam to supply universal safety since gp41 mediates viral fusion both in cell-free and cell-associated HIV-1 transmitting 3rd party of co-receptor subtype [4-6]. (biomasswars.com)

HIV stands for human immunodeficiency virus. (medlineplus.gov)
Forensic microbiology is a scientific area that has emerged with the need to investigate biocrimes, as in the case of intentional transmission of the Human Immunodeficiency Virus (HIV). (scielo.sa.cr)
The reduction in mother-to-child transmission of human immunodeficiency virus (HIV) is regarded as one of the most effective public health initiatives in the United States. (medscape.com)
have occupational exposure to blood and other body fluids that might contain human immunodeficiency virus (HIV). (cdc.gov)
Women should be counseled that consistent and correct use of the male latex condom reduces the risk for transmission of human immunodeficiency virus (HIV) and other sexually transmitted diseases (STDs). (cdc.gov)

This prevents HIV from copying itself, which reduces the amount of HIV in the body. (medlineplus.gov)
Blocking either of these molecules prevents HIV from entering the cells. (medlineplus.gov)
This prevents HIV from entering the cell. (medlineplus.gov)
The fusion inhibitor prevents the membrane of the host CD4 cell from fusing with the HIV envelope. (uspharmacist.com)

Multidrug-resistant (MDR) HIV refers to strains of HIV with reduced susceptibility to drugs within all three classes of antiretroviral therapies (ARTs). (managedhealthcareexecutive.com)
2,4,5 Transmission of multi-drug-resistant strains of HIV is rare. (managedhealthcareexecutive.com)

During the second step in the HIV life cycle, the HIV envelope fuses with the CD4 cell membrane, allowing the viral genetic material to enter the host cell. (uspharmacist.com)
That is accompanied by condensation of two helical areas within gp41, leading to formation of the six helix package, facilitating close get in touch with from the viral and sponsor membranes and accompanied by fusion from the viral envelope using the cell membrane. (bioinbrief.com)

The strategy is targeted primarly to improve the pharmacokinetic properties from the fusion peptide by covalent linkage for an antibody. (bioinbrief.com)

The greatest risk factor for vertical transmission is thought to be advanced maternal disease, likely due to a high maternal HIV viral load. (medscape.com)

RET fusion positivity, as determined by a Clinical Laboratory Improvement Amendments or equivalently certified next generation sequencing (NGS) assay (tissue or blood). (who.int)

2005. Protection of macaques from vaginal SHIV challenge by vaginally delivered inhibitors of virus-cell fusion. . (cornell.edu)

The IC50 values for T-1249 against each of SHIV-162P3 (R5) SHIV-89.6P (R5X4) and SHIV-KU1 (X4) ranged from 0.77 to 3.9 nM which is consistent with the reported potencies for this peptide against a range of HIV-1 isolates in similar assays (see below). (sciencepop.org)
HIV isolates that use CXCR4 are traditionally known as T-cell tropic isolates. (wikidoc.org)

QadirVID-19: He designed a fusion inhibitor for specific treatment of COVID-19, which was named as QadirVID-19. (wikipedia.org)
The treatment of HIV with medicines is called antiretroviral therapy (ART). (medlineplus.gov)
If you miss doses or don't follow a regular schedule, your treatment may not work, and the HIV virus may become resistant to the medicines. (medlineplus.gov)
POT includes performing post Dual antiplatelet therapy (DAPT) using a combination treatment of aspirin with a P2Y12 platelet inhibitor after percutaneous coronary intervention (PCI), reduces the risk of stent thrombosis and ischemic cardiac events, but increases the risk of best Online Pharmacies Buy Vibramycin complications. (ddtpsod.com)
Treatment must be planned and adjusted for every individual person with HIV. (health.am)
Eligible subjects are chronic HIV-1 infected patients who have never been treated with antiretroviral treatment and for whom there is no need to start antiretroviral treatment. (druglib.com)
Before the current treatment era, approximately 2000 babies were infected with HIV each year in the United States alone. (medscape.com)
See "Selecting antiretroviral regimens for treatment-naïve persons with HIV-1: General approach", section on 'Considerations prior to initiating treatment' and "Evaluation of the treatment-experienced patient failing HIV therapy" . (medilib.ir)
HIV treatment guidelines recommend a genotypic assay be the preferred testing method in treatment-naïve patients [ 4,7-10 ]. (medilib.ir)
Further information can be found at HIV Treatment Regimens CDC Guidelines, Adult/Adolescent . (medscape.com)

To infect a cell, HIV has to bind to two types of molecules on the cell's surface. (medlineplus.gov)
People infected with HIV who are receiving therapy can still infect others through unprotected sex and needle-sharing. (rxwiki.com)
The result is immature, defective HIV that does not infect new cells. (msdmanuals.com)

Qadirvirtide and Qadir-C30: His work also includes invention of anti-HIV drugs, Qadirvirtide and Qadir-C30. (wikipedia.org)
Many of the antiretroviral drugs that have been approved for HIV-infected adults and adolescents are gaining FDA approval for use in younger children. (medscape.com)

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Dissection of human immunodeficiency virus type 1 entry with neutralizing antibodies to gp41 fusion intermediates. (1/304)

Human CD38 interferes with HIV-1 fusion through a sequence homologous to the V3 loop of the viral envelope glycoprotein gp120. (2/304)

Enfuvirtide, an HIV-1 fusion inhibitor, for drug-resistant HIV infection in North and South America. (3/304)

Efficacy of enfuvirtide in patients infected with drug-resistant HIV-1 in Europe and Australia. (4/304)

A small molecule HIV-1 inhibitor that targets the HIV-1 envelope and inhibits CD4 receptor binding. (5/304)

The entry of entry inhibitors: a fusion of science and medicine. (6/304)

Putative role of membranes in the HIV fusion inhibitor enfuvirtide mode of action at the molecular level. (7/304)

Enfuvirtide (T-20): a novel human immunodeficiency virus type 1 fusion inhibitor. (8/304)

HIV Fusion Inhibitors

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Dissection of human immunodeficiency virus type 1 entry with neutralizing antibodies to gp41 fusion intermediates. (1/304)

Human CD38 interferes with HIV-1 fusion through a sequence homologous to the V3 loop of the viral envelope glycoprotein gp120. (2/304)

Enfuvirtide, an HIV-1 fusion inhibitor, for drug-resistant HIV infection in North and South America. (3/304)

Efficacy of enfuvirtide in patients infected with drug-resistant HIV-1 in Europe and Australia. (4/304)

A small molecule HIV-1 inhibitor that targets the HIV-1 envelope and inhibits CD4 receptor binding. (5/304)

The entry of entry inhibitors: a fusion of science and medicine. (6/304)

Putative role of membranes in the HIV fusion inhibitor enfuvirtide mode of action at the molecular level. (7/304)

Enfuvirtide (T-20): a novel human immunodeficiency virus type 1 fusion inhibitor. (8/304)

Enzymatic triggered release of an HIV-1 entry inhibitor from prostate specific antigen degradable microparticles

Investigational drugs in HIV: Pros and cons of entry and fusion inhibitors (Review)

Muhammad Imran Qadir - Wikipedia

HR212 inhibits HIV-1 access by blocking cell-cell fusion The fusion - Inhibition of autophagy with dual PI3K/mTOR inhibitors

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