The regulation of human immunodeficiency virus type 1 infection and replication in primary monocytes was investigated by mutagenesis of recombinant proviral clones containing an env determinant required for the infectivity of monocytes. Virus replication was assayed by determination of reverse transcriptase activity in culture fluids and by recovery of virus from monocytes following cocultivation with uninfected peripheral blood mononuclear cells. Three virus replication phenotypes were observed in monocytes: productive infection, silent infection, and no infection. Incorporation of the monocytetropic env determinant in a full-length clone incapable of infection or replication in primary monocytes (no infection) conferred the capacity for highly efficient virus replication in monocytes (productive infection). Clones with the env determinant but lacking either functional vpr or vpu genes generated lower replication levels in monocytes. Mutation of both vpr and vpu, however, resulted in nearly complete
Using the one-step growth technique the production of the virus T2 in its host, measured by latent period and burst size, was shown to depend on the nutritional environment of the host cell.. When E. coli, grown in broth, was transferred to a simple medium, single organic compounds such as some amino acids and nucleosides were found to increase or accelerate the synthesis of virus.. An antimetabolite of glutamic acid, an amino acid important for virus synthesis, was shown to be inhibitory.. Several naturally occurring amino acids, leucine, serine, and cysteine, inhibited virus synthesis in the simple medium.. A chemically defined mixture was found which supported a rate of virus synthesis very nearly comparable to that found for host cells in nutrient broth.. ...
Yes, this methods works when you know the virus you are incubating and have the right cells available. if you dont know what celltype your virus infects, youll have to try some systems, till you find one that supports virus replication in vitro ...
A single virus particle (virion) cannot replicate or express genetic material (DNA, RNA) without a host cell. Viral infection and virus replication involves six…
To investigate the effect of NP-41V and/or 210D on virus replication, recombinant viruses were generated with reverse-genetics as described previously [21]. For biosafety concerns, the four rescued viruses were performed using G1 (H9N2) backbones: rgG1-WT, rgG1-NP-V41I, rgG1-D210E, and rgG1- NP-V41I-D210E. MDCK cells were infected with rescued viruses at a multiplicity of infection (MOI) of 0.001, and incubated in the appropriate medium containing 2 mg/L N-p-tosyl-L-phenylalaninechloromethyl ketone-treated (TPCK) trypsin (Sigma, Saint Louis, MO, USA) at 33 or 37°C. At 12, 24, 48, 72, and 96 hours post inoculation (hpi), supernatants were harvested and virus titers were determined using MDCK cells, as described previously [22]. As shown in Figure 3B, at 37°C, the D210E substitution in the NP protein significantly decreased the replication ability of rgG1-WT at early stages post infection (12 and 24 hpi (p , 0.05; n = 3), although all four viruses demonstrated comparable growth capability at ...
Endothelial cells are believed to play an important role in response to virus infection. Our previous microarray analysis showed that H9N2 virus infection and inactivated viral particle inoculation increased the expression of interferon-inducible transmembrane protein 1 (IFITM1) in human umbilical vein endothelial cells (HUVECs). In present study, we deeply investigated the expression patterns of IFITM1 and IFITM1-mediated antiviral response induced by H9N2 virus infection and inactivated viral particle inoculation in HUVECs. Epithelial cells that are considered target cells of the influenza virus were selected as a reference control. First, we quantified the expression levels of IFITM1 in HUVECs induced by H9N2 virus infection or viral particle inoculation using quantitative real-time PCR and western blot. Second, we observed whether hemagglutinin or neuraminidase affected IFITM1 expression in HUVECs. Finally, we investigated the effect of induced-IFITM1 on the antiviral state in HUVECs by siRNA and
Mathematicians and scientists from two UK universities have collaborated to shed new light on the process of viral replication during an infection.. Experimentalists from the University of Leeds and mathematicians from the University of York devised a mathematical model that gives new insights into the molecular mechanisms behind virus assembly, helping to explain the efficiency of their operation.. Researchers from the Departments of Mathematics and Biology at the University of York have developed a theoretical basis for the speed and efficiency with which viruses assemble the protective proteins for their genetic information - in this case an RNA molecule - during an infection.. The team incorporated multiple specific contacts between the genomic RNA and the proteins in the containers, along with other details of real virus infections, into a mathematical model that demonstrates how these contacts act collectively to reduce the complexity of virus formation.. They thus solved a longstanding ...
The objective: Binding viruses to designer ViroCatcher cells that cannot support viral replication to diagnose, attenuate, and prevent infection. What we intended to do: (1) Make our designer cell safe, (2) Express specific cell surface receptors and antibodies to catch the virus, (3) Transduce the signal after viruses attached for feedback control, and (4) Remove the viruses along with ViroCatcher itself. Anticipated results: the ViroCatcher is made safe for the bloodstream. When it is injected into the bloodstream, our ViroCatcher passively lies around letting viruses attach to it by using its 4 receptors: CD4 (for HIV), Integrin (for various viruses), Sialic Acid (for Influenza), and Antibodies (for Influenza). After enough viruses attach to it, or after a certain amount of time elapses, it removes itself from the bloodstream by calling macrophages to eat it up. ...
IFITMs are broad antiviral factors that block incoming virions in endosomal vesicles, protecting target cells from infection. In the case of HIV-1, we and others reported the existence of an additional antiviral mechanism through which IFITMs lead to the production of virions of reduced infectivity. However, whether this second mechanism of inhibition is unique to HIV or extends to other viruses is currently unknown. To address this question, we have analyzed the susceptibility of a broad spectrum of viruses to the negative imprinting of the virion particles infectivity by IFITMs. The results we have gathered indicate that this second antiviral property of IFITMs extends well beyond HIV and we were able to identify viruses susceptible to the three IFITMs altogether (HIV-1, SIV, MLV, MPMV, VSV, MeV, EBOV, WNV), as well as viruses that displayed a member-specific susceptibility (EBV, DUGV), or were resistant to all IFITMs (HCV, RVFV, MOPV, AAV). The swapping of genetic elements between resistant ...
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Recent studies have shown that replication of hepatitis C virus (HCV) is dependent on miR-122 expression.[20] miR-122 regulates HCV by binding directly to two adjacent sites close to the 5 end of HCV RNA.[21] Although these experiments were conducted using genotype 1a and 1b HCV RNA, the miR-122 binding sites are highly conserved across different genotypes, and miR-122 is also required for replication of infectious type 2a HCV.[22] As miRNAs generally function to repress gene expression by binding to 3UTR sites, this positive regulation of viral replication via a 5UTR represents a novel function for miR-122. The mechanism of regulation is not yet clear. miR-122 stimulates translation of HCV RNA, but not to a sufficient extent to explain its effects on viral replication, indicating that a second stage of the viral replication cycle must also be regulated.[23][24] HCV RNA synthesis is not affected by miR-122, suggesting that regulation of other processes such as RNA stability may occur.[25][26] ...
In vertebrates, successful host defense against viral infections relies heavily on the early production of IFN-α/β, which promotes an antiviral state in adjacent noninfected cells as well as the activation of antiviral cytotoxic lymphocytes (1). IL-12 and TNF-α are also critical cytokines involved in antiviral defense. IL-12 stimulates the proliferation of T cells as well as the production of IFN-γ by both NK and T cells, whereas TNF-α takes part in the activation of cellular immunity and in the induction of apoptosis of infected cells. Plasmacytoid dendritic cells (pDCs)3 have been shown to be specialized in the production of high levels of IFN-α/β and TNF-α in response to a wide variety of viruses in both humans and mice (2).. The molecular mechanisms promoting the production of cytokines by pDCs in response to most viral infections are independent of productive viral replication within the pDC itself and rely on the detection of viral genomes from engulfed viral particles or apoptotic ...
Viruses need living cells for replication and production of virus progeny. Thus far, antiviral therapy primarily targets viral factors but often induces therapy resistance. New improved therapies attempt to targets cellular factors that are essential for viral replication.
Reproduction in Viruses or Replication of viruses are obligate intracellular parasite. They are reproduced only within a host cell. Viruses lack the enzyme for its replication. After reading this article you will know that how do viruses reproduce and its life cycle.
The genotype and phenotype of HSV2-gD27 are stable when the virus is passaged in human epithelial cells in vitro and during acute infection of mice.. HSV2-gD27 was propagated in B78H1-A10 mouse cells, which express human HVEM but not human nectin-1. HSV2-gD27 was not able to infect B78H1-C10 mouse cells, which express human nectin-1 but not HVEM, since the mutation in gD prevents its interaction with nectin-1 (33). To determine the sensitivity of the assay to detect WT virus mixed with HSV2-gD27, we infected B78H1-C10 cells with 400 PFU of WT virus (titrated in ARPE-19 cells) and 106 PFU of HSV2-gD27 (also titrated in ARPE-19 cells), either together or separately, and assayed the number of plaques on B78H1-C10 cells, which support replication of WT virus but not HSV2-gD27. Coinfection of B78H1-C10 cells with the two viruses resulted in a mean of 6.5 plaques, infection with WT virus alone yielded 5.5 plaques, and infection with HSV2-gD27 yielded no plaques. These data indicate that HSV2-gD27 does ...
PositivelyPositive.ca is designed to create awareness around the many HIV and AIDS issues and promotes messages of positive living with HIV
RNase L is a principle mediator of the innate antiviral response and is thus critically important for human health. Virus replication in higher vertebrates is r...
The search for inhibitors of viral replication is dependent on understanding the events taking place at the molecular level during viral infection. All the essential steps during the viral life cycle...
There are more than 25 drugs to control HIV, yet the virus remains one of the worlds biggest health problems. One of the many challenges with existing therapies is that a dormant version of the virus is always lurking in the background, ready to attack the immune system as soon as treatment is interrupted. _______________________________________…
The reason for using drugs from different families is because there is evidence of cross-resistance. That is, if a strain of HIV can defeat one NNRTI it might show resistance to all NNRTIs. An analogy to delaying resistance by administering three different classes of drugs simultaneously is that most people are capable of bunny hopping up one stair-step. Very few are capable of bunny hopping directly to the third step in one hop. In a similar way, a virus might mutate by random chance to defeat one antiviral mechanism. The chances of a virus simultaneously experiencing three mutations that defeat all three antiviral mechanisms is very, very ...
Hi! I am new around here but wanted to see if anyone else is using IVFAdvantage or Attain? I considered both but went with IVFAdvantage because I like
Plants have evolved very good defenses against viruses over the millennia, and we can take advantage of these natural protections against viruses for ourselves.
Plants have evolved very good defenses against viruses over the millennia, and we can take advantage of these natural protections against viruses for ourselves.
Scientists at the Gladstone Institutes discovered that an enzyme called SMYD2 could be a new therapeutic target for flushing out the HIV that hides in infected individuals. Overcoming this latent virus remains the most significant ...
Viruses are small infectious particles that cannot replicate on their own, but need to infect a cell in order to copy. Viral particles (called virions) consist of a protein envelope and a genetic material inside.
Panda Antivirus has found the following viruses in the message: Server : EXCHANGE02 Sent by : [email protected] Address : [email protected] To : [email protected] Subject : Re: Re: My details Date : 05/09/2003 08:48:07 Sent by You File : details.pif Virus : W32/Sobig.F - Deleted http://www.pandasoftware.com ...
One digit Multiplication Activity 4. Free online multiplication activities to help kids learn the multiplication facts. 1st grade year 1 multiplication.
TY - BOOK. T1 - Viral genome replication. AU - Cameron, Craig Eugene. AU - Raney, Kevin D.. AU - Götte, Matthias. PY - 2009/1/1. Y1 - 2009/1/1. N2 - Provides the first comprehensive review of viral genome replication strategies, emphasizing not only pathways and regulation but also the structure-function, mechanism, and inhibition of proteins and enzymes required for this process Currently, there is no single source that permits comparison of the factors, elements, enzymes and/or mechanisms employed by different classes of viruses for genome replication. As a result, we (and our students) often restrict our focus to our particular system, missing out on the opportunity to define unifying themes in viral genome replication or benefit from the advances in other systems. For example, extraordinary biological and experimental paradigms that have been established over the past five years for the DNA replication systems of bacteriophage T4 and T7 will likely be of great value to anyone interested in ...
In vitro fitness assays are essential tools for determining viral replication fitness for viruses such as HIV-1. Various measurements have been used to extrapolate viral replication fitness, ranging from the number of viral particles per infectious unit, growth rate in cell culture, and relative fitness derived from multiple-cycle growth competition assays. Growth competition assays provide a particularly sensitive measurement of fitness since the viruses are competing for cellular targets under identical growth conditions. There are several experimental factors to consider when conducting growth competition assays, including the multiplicity of infection (MOI), sampling times, and viral detection and fitness calculation methods. Each factor can affect the end result and hence must be considered carefully during the experimental design. The protocol presented here includes steps from constructing a new recombinant HIV-1 clone to performing growth competition assays and analyzing the experimental ...
My research interests are centered on viruses, particularly influenza viruses, which are important human and animal pathogens causing widespread clinical and veterinary disease. My group focuses on the fundamental molecular mechanisms of influenza virus replication, aiming to understand the molecular determinants of host range and virulence of influenza viruses. By gaining further insights into the molecular aspects of influenza virus replication we hope to facilitate the development of novel strategies to combat influenza.. Specifically, we address questions ranging from how the influenza virus RNA polymerase transcribes and replicates the segmented negative-sense viral RNA genome in the nucleus of the infected cell to how the RNA genome is exported from the nucleus and assembles into infectious progeny virus particles. We are also interested in the role of host factors in viral replication as well as in understanding the effects of virus infection on the host cell, the molecular mechanisms of ...
RNA virus replication machineries.(A) RdRps of hepatitis C virus and reovirus. Hepatitis C virus is a (+)RNA virus from the Flaviviridae family, while reovirus
Viral and cellular factors responsible for parvovirus target cell specificity have been examined for two serologically indistinguishable strains of the minute virus of mice which infect mouse cells of dissimilar differentiated phenotype. Both the prototype strain and the immunosuppressive strain grow in and form plaques on monolayers of simian virus 40-transformed human fibroblasts, a finding that has allowed the comparison of several aspects of their virus-host cell interactions. Although closely related by antigenic and genomic criteria, both the prototype strain and the immunosuppressive strain are restricted for lytic growth in each others murine host cell, that is, in T cells and fibroblasts, respectively. The host range of each virus variant appears to be specified by a genetic determinant that is stably inherited in the absence of selection. In the restrictive virus-host interaction lytic growth is limited to a small or, in some cases, undetectable subset of the host cell population, and ...
figure 19.4. Adjunctive treatments of HIV-1 and other neurodegenerative disorders. A number of adjunctive therapies are being developed for treatment of HIV-1-associated cognitive impairments. These are directed at pathogenic mechanisms for disease, including those that affect viral replication, modulate neuroinflammation, interdict cell signaling events that lead to neuronal demise, or affect cell migration into the brain or the viral replication cycle (A). Novel approaches are now under development to harness the hosts own immune system to combat disease. These methodologies currently involve direct immunization strategies and novel nanoparticle delivery systems (B). GA, glatiramer acetate; MDM, monocyte derived macrophages; MP, mononuclear phagocyte; PAF, platelet-activating factor; PPARg, peroxisome proliferator-activated receptor gamma.. multifactorial, in that a complex set of toxic reactions including inflammation, glutamatergic neurotoxicity, increases in iron and nitric oxide, ...
The identification of novel antiretroviral agents is required to provide alternative treatment options for HIV-1-infected patients. The screening of a phenotypic cell-based viral replication assay led to the identification of a novel class of 4,5-dihydro-1H-pyrrolo[3,4-c]pyrazol-6-one (pyrrolopyrazolone) HIV-1 inhibitors, exemplified by two compounds: BI-1 and BI-2. These compounds inhibited early postentry stages of viral replication at a step(s) following reverse transcription but prior to 2 long terminal repeat (2-LTR) circle formation, suggesting that they may block nuclear targeting of the preintegration complex. Selection of viruses resistant to BI-2 revealed that substitutions at residues A105 and T107 within the capsid (CA) amino-terminal domain (CANTD) conferred high-level resistance to both compounds, implicating CA as the antiviral target. Direct binding of BI-1 and/or BI-2 to CANTD was demonstrated using isothermal titration calorimetry and nuclear magnetic resonance (NMR) chemical ...
Inhibition of HIV-1 progeny virion release by cell-surface CD4 is relieved by expression of the viral Nef protein.s profile, publications, research topics, and co-authors
Abstract: A successful infection by a plant virus results from the complex molecular interplay between the host plant and the invading virus. Thus, dissecting the molecular network of virus-host interactions advances the understanding of the viral infection process and may assist in the development of novel antiviral strategies. In the past decade, molecular identification and functional characterization of host factors in the virus life cycle, particularly single-stranded, positive-sense RNA viruses, have been a research focus in plant virology. As a result, a number of host factors have been identified. These host factors are implicated in all the major steps of the infection process. Some host factors are diverted for the viral genome translation, some are recruited to improvise the viral replicase complexes for genome multiplication, and others are components of transport complexes for cell-to-cell spread via plasmodesmata and systemic movement through the phloem. This review summarizes ...
Transcription mapping studies and DNA sequence analysis of the vaccinia virus HindIII D fragment predict that gene D8 encodes a protein 304 amino acids in length, with a molecular mass of 35,426 daltons, that is expressed at late times in infection. In order to determine whether the native D8 protein is required for virus propagation, we constructed a frameshift mutation in the D8 coding sequence. Virus containing this mutation were isolated and shown to replicate in a single-step growth experiment with wild type virus growth kinetics, demonstrating that the normal-length D8 protein is not essential for virus propagation in tissue culture. In order to investigate the synthesis of the wild-type and the mutant D8 proteins in virus-infected cells, we raised polyclonal antisera to a fusion protein consisting of a portion of the D8 coding sequence linked to the Escherichia coli trpE gene. Western blot (immunoblot) analysis of the time course of D8 protein synthesis in cells infected with either ...
Insight on Protein That Blocks HIV Replication May Help Battle Viral Reservoir April 22, 2013 Insight on Protein That Blocks HIV Replication May Help Battle Viral Reservoir Re, team37262board
In Part III of our series on "Strategies for Improving Viral Yield in Vaccine Manufacturing," we will examine the use of manufacturing strategies to improve viral yield and lower cost of production. Improving viral yield and lowering cost is critical for improving access to vaccines in the developing world where even minor medical expenses are prohibitive. Improving viral yield also enables a faster response time in case of a pandemic. Improving cell culture media is one way to increase virus yield and was examined in Part I titled "Improving Media to Increase Virus Yield in Vaccine Production." In Part II titled "Utilizing Bioreactors to Increase Virus Production in Vaccine Manufacturing," we discussed the role of bioreactors and accompanying technology as another way to achieve higher yield. In Part III we will look at additional strategies that can be employed as part of the manufacturing process to achieve higher yield and reduce cost.. In vaccine manufacturing keeping viruses stable during ...
We believe that it is necessary to address each of these problem areas in order to deliver a successful curative combination therapy for HBV. Any such cure needs to rapidly, completely and sustainably reduce HBV viral load to undetectable levels, stimulate and reactivate the patients immune response in order to enable the body to fight HBV, and inhibit the formation of and eliminate viral cccDNA in the infected liver cells.. Aggressive Suppression of HBV Replication. Determining the level of viral replication at the site of infection in the liver is difficult and invasive. Because of this, alternative measurements, which utilize blood as a surrogate, are typically used. This is not ideal, because significantly more virus can be found in the liver than in the bloodstream. Although current HBV therapies do lead to undetectable virus levels in the blood in some infected patients, it is believed that low-level viral replication continues to occur in infected liver cells. The likelihood of ...
English: A simplified diagram of the Hepatitis C virus replication cycle. Created by User:GrahamColm (Photo credit: Wikipedia) ...
In a study published Wednesday in Nature Communications, researchers discovered that certain strains of H7N9 have mutated to become highly resistant to antivirals like Tamiflu while maintaining high levels of pathogenicity. This is not normal. Normally when a virus acquires drug-resistance through mutation, this mutation attenuates it, decreasing viral virulence or replication ability. The study…
A variety of different methods for the evaluation of antiviral agents in cell culture systems are briefly reviewed. It has been repeatedly noted that many test conditions such as the cell culture system, virus strain, virus challenge dose, virus input multiplicity of infection, and time of harvesting, etc., can substantially affect or even alter the test results, thus making comparative studies and unambiguous evaluations very difficult. Attempts are made to discuss previous test methods together with our recent studies with the aim to simplify test procedures and assay methods. Suggestions are proposed for in vitro evaluation of new antiviral agents. It is hoped that this review will alarm investigators to the problems of assaying new antiviral agents. If the suggestions made in this review can be followed, the screening of the enormous number of promising antiviral compounds may be made more efficiently in the near future.
... blue-green alga Spirulina, exhibits activity against a variety of viruses.
Accumulation of viral products such as RNA replication intermediates and viral proteins represents a potential stressor for host cells. Rapidly after detection, host cells respond by implementing multiple appropriated defense mechanisms, including innate immune and stress responses. The strongest response to several forms of stress, including viral infections, is a global reduction of protein synthesis which promotes cellular survival. Translation suppression is induced by the phosphorylation of the alpha subunit of the eukaryotic translation initiation factor-2 (eIF2α), thereby causing stalling of translation initiation and accumulation of stalled pre-initiation complexes in cytosolic stress granules (SGs). Viruses do not package ribosomes and therefore fully rely on the utilization of the host translation machinery to ensure viral protein synthesis, replication and virus progeny production. As a consequence, virus survival depends on the establishment of a delicate and fine-tuned balance ...
Molecular Plant-Microbe Interactions 23:283-293...Ken Komatsu,1 Masayoshi Hashimoto,1 Johji Ozeki,1 Yasuyuki Yamaji,1 Kensaku Maejima,1 Hiroko Senshu,1 Misako Himeno,1 Yukari Okano,1 Satoshi Kagiwada,2 and Shigetou Namba1...
Vaccines have provided considerable success in preventing viral disease, but they have modest or no therapeutic effect for individuals who are already infected. Consequently, our second arm of antiviral defense has been the development and use of antiviral drugs: they can stop an infection once it has started.. However, despite 50 years of research, our arsenal of antiviral drugs is dangerously small. Only about 30 antiviral drugs are available on the US market, most against herpesviruses and HIV-1. There are many reasons for this paucity of antiviral drugs. Compounds interfering with virus growth can adversely affect the host cell, leading to unacceptable toxicity. Many medically important viruses are dangerous, cannot be propagated in the laboratory or tested in animal systems. Another requirement often difficult to fulfill is that the drugs must completely block virus replication. Many acute virus infections are of short duration; by the time the patient feels ill, virus replication is ...
As shown above, early phase II studies strongly suggest that RBV is needed in protease inhibitor drug regimens. Patients who did not receive RBV in the PROVE trials and those with low-dose RBV (400-1000 mg) in the SPRINT-1 trial had increased viral breakthrough, higher relapse and lower SVR. This data strongly indicates that standard-dose RBV is needed to optimize response to these first generation protease inhibitors by reducing the development of resistance/breakthrough. It is also clear that the initial rapid decrease in HCV viral levels with protease combination therapy is because of inhibition of wild type virus that then leads to the uncovering of pre-existing resistant variants. Resistant variants are present in most patients at very low rates (,1%) and are usually detected after near complete suppression of the dominant, wild type virus. The continued replication of these variants can then lead to a virological breakthrough. To date, mutations conferring TVR-resistance have been ...
Viruses are among the simplest biological systems and are highly effective vehicles for the delivery of genetic material into susceptible host cells. Artificial viruses can be used as model systems for providing insights into natural viruses and can be considered a testing ground for developing artificial life. Moreover, they are used in biomedical and biotechnological applications, such as targeted delivery of nucleic acids for gene therapy and as scaffolds in material science. In a natural setting, survival of viruses requires that a significant fraction of the replicated genomes be completely protected by coat proteins. Complete protection of the genome is ensured by a highly cooperative supramolecular process between the coat proteins and the nucleic acids, which is based on reversible, weak and allosteric interactions only. However, incorporating this type of supramolecular cooperativity into artificial viruses remains challenging. Here, we report a rational design for a self-assembling ...