A species of ARENAVIRUS, one of the New World Arenaviruses (ARENAVIRUSES, NEW WORLD), causing a fatal infection in the cricetine rodent Oryzomys albigularis. Asymptomatic laboratory infection in humans has been reported.
A family of RNA viruses naturally infecting rodents and consisting of one genus (ARENAVIRUS) with two groups: Old World Arenaviruses (ARENAVIRUSES, OLD WORLD) and New World Arenaviruses (ARENAVIRUSES, NEW WORLD). Infection in rodents is persistent and silent. Vertical transmission is through milk-, saliva-, or urine-borne routes. Horizontal transmission to humans, monkeys, and other animals is important.
One of two groups of viruses in the ARENAVIRUS genus and considered part of the New World complex. It includes JUNIN VIRUS; PICHINDE VIRUS; Amapari virus, and Machupo virus among others. They are the cause of human hemorrhagic fevers mostly in Central and South America.
Diseases caused by American hemorrhagic fever viruses (ARENAVIRUSES, NEW WORLD).
Virus diseases caused by the ARENAVIRIDAE.
A group of viral diseases of diverse etiology but having many similar clinical characteristics; increased capillary permeability, leukopenia, and thrombocytopenia are common to all. Hemorrhagic fevers are characterized by sudden onset, fever, headache, generalized myalgia, backache, conjunctivitis, and severe prostration, followed by various hemorrhagic symptoms. Hemorrhagic fever with kidney involvement is HEMORRHAGIC FEVER WITH RENAL SYNDROME.
Viruses whose genetic material is RNA.
Ribonucleic acid that makes up the genetic material of viruses.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
The type species of ARENAVIRUS, part of the Old World Arenaviruses (ARENAVIRUSES, OLD WORLD), producing a silent infection in house and laboratory mice. In humans, infection with LCMV can be inapparent, or can present with an influenza-like illness, a benign aseptic meningitis, or a severe meningoencephalomyelitis. The virus can also infect monkeys, dogs, field mice, guinea pigs, and hamsters, the latter an epidemiologically important host.
Proteins found in any species of virus.
Established cell cultures that have the potential to propagate indefinitely.
Substances elaborated by viruses that have antigenic activity.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
The only genus in the family ARENAVIRIDAE. It contains two groups ARENAVIRUSES, OLD WORLD and ARENAVIRUSES, NEW WORLD, which are distinguished by antigenic relationships and geographic distribution.

Sequence analysis of the small RNA segment of guinea pig-passaged Pichinde virus variants. (1/39)

The established animal model for Lassa fever is based on the new world arenavirus Pichinde (PIC). Natural isolates of PIC virus are attenuated in guinea pigs, but serial guinea pig passage renders them extremely virulent in that host. We have compared the nucleotide sequences of the small RNA segments of two attenuated, low-passage variants of the PIC virus Munchique strain (CoAn 4763) and two virulent, high-passage derivatives. Missense mutations in the glycoprotein precursor (GPC) gene at codons GPC-119, GPC-140, and GPC-164 and the nucleoprotein gene (NP) codons NP-35 and NP-374 were most closely associated with virulence. Codon GPC-140 is predicted to represent a region of peak hydrophilicity of the glycoprotein 1 (GP1); it is conceivable that mutations at this site could influence virulence by altering B cell epitopes or virus attachment protein conformation.  (+info)

Attrition of T cell memory: selective loss of LCMV epitope-specific memory CD8 T cells following infections with heterologous viruses. (2/39)

Using a variety of techniques, including limiting dilution assays (LDA), intracellular IFNgamma assays, and Db-IgG1 MHC dimer staining to measure viral peptide-specific T cell number and function, we show here that heterologous virus infections quantitatively delete and qualitatively alter the memory pool of T cells specific to a previously encountered virus. We also show that a prior history of a virus infection can alter the hierarchy of the immunodominant peptide response to a second virus and that virus infections selectively reactivate memory T cells with distinct specificities to earlier viruses. These results are consistent with a model for the immune system that accommodates memory T cell populations for multiple pathogens over the course of a lifetime.  (+info)

Virus-induced abrogation of transplantation tolerance induced by donor-specific transfusion and anti-CD154 antibody. (3/39)

Treatment with a 2-week course of anti-CD154 antibody and a single transfusion of donor leukocytes (a donor-specific transfusion or DST) permits skin allografts to survive for >100 days in thymectomized mice. As clinical trials of this methodology in humans are contemplated, concern has been expressed that viral infection of graft recipients may disrupt tolerance to the allograft. We report that acute infection with lymphocytic choriomeningitis virus (LCMV) induced allograft rejection in mice treated with DST and anti-CD154 antibody if inoculated shortly after transplantation. Isografts resisted LCMV-induced rejection, and the interferon-inducing agent polyinosinic:polycytidylic acid did not induce allograft rejection, suggesting that the effect of LCMV is not simply a consequence of nonspecific inflammation. Administration of anti-CD8 antibody to engrafted mice delayed LCMV-induced allograft rejection. Pichinde virus also induced acute allograft rejection, but murine cytomegalovirus and vaccinia virus (VV) did not. Injection of LCMV approximately 50 days after tolerance induction and transplantation had minimal effect on subsequent allograft survival. Treatment with DST and anti-CD154 antibody did not interfere with clearance of LCMV, but a normally nonlethal high dose of VV during tolerance induction and transplantation killed graft recipients. We conclude that DST and anti-CD154 antibody induce a tolerant state that can be broken shortly after transplantation by certain viral infections. Clinical application of transplantation tolerance protocols may require patient isolation to facilitate the procedure and to protect recipients.  (+info)

Alterations in NF-kappaB and RBP-Jkappa by arenavirus infection of macrophages in vitro and in vivo. (4/39)

Pichinde virus is an arenavirus that infects guinea pigs and serves as an animal model for human Lassa fever. An attenuated Pichinde virus variant (P2) and a virulent variant (P18) are being used to delineate pathogenic mechanisms that culminate in shock. In guinea pigs, the infection has been shown to begin in peritoneal macrophages following intraperitoneal inoculation and then spreads to the spleen and other reticuloendothelial organs. We show here that infection of the murine monocytic cell line P388D1 with either Pichinde virus variant resulted in the induction of inflammatory cytokines and effectors, including interleukin-6 and tumor necrosis factor alpha. Since these genes are regulated in part by the cellular transcription factors NF-kappaB and RBP-Jkappa, we compared the activities of NF-kappaB and RBP-Jkappa in P388D1 cells following infection with Pichinde virus. The attenuated P2 virus inhibited NF-kappaB activation and caused a shift in the size of the RBP-Jkappa complex. The virulent P18 virus showed less inhibition of NF-kappaB and failed to alter the size of the RBP-Jkappa complex. Peritoneal cells from P2-infected guinea pigs showed induction of NF-kappaB RelA/p50 heterodimer and p50/p50 homodimer and manifested an increase in the size of RBP-Jkappa. By contrast, P18 induced large amounts of the NF-kappaB p50/p50 dimer but failed to induce RelA/p50 or to cause an increase in the RBP-Jkappa size. Taken together, these changes suggest that the attenuated viral strain induces an "activation" of macrophages, while the virulent form of the virus does not.  (+info)

Reassortant analysis of guinea pig virulence of pichinde virus variants. (5/39)

The new world arenavirus Pichinde (PIC) is the basis of an accepted small animal model for human Lassa fever. PIC (Munchique strain) variant P2 is attenuated in guinea pigs, whereas variant P18 is extremely virulent. Previous sequence analysis of the S segments of these two viruses indicated a small number of possible virulence markers in the glycoprotein precursor (GPC) and nucleoprotein (NP) genes. In order to determine the role of these S segment genes in guinea pig virulence in this system, we have generated reassortant viruses. When tested in outbred guinea pigs, the reassortant containing the S segment from the virulent parent P18 (S18L2) caused significantly higher morbidity than the reciprocal reassortant. This increased morbidity was associated with higher viral titers in serum and spleen. However, the S18L2 reassortant was not as fully virulent in this system as the P18 parent, indicating a role for L segment genes in virulence.  (+info)

Dynamics of memory T cell proliferation under conditions of heterologous immunity and bystander stimulation. (6/39)

By examining adoptively transferred CSFE-labeled lymphocytic choriomeningitis virus (LCMV)-immune donor T cells in Thy-1 congenic hosts inoculated with viruses or with the cytokine inducer poly(I:C), strikingly different responses of bona fide memory T cells were found in response to different stimuli. Poly(I:C) (cytokine) stimulation caused a limited synchronized division of memory CD8 T cells specific to each of five LCMV epitopes, with no increase and sometimes a loss in number, and no change in their epitope hierarchy. Homologous LCMV infection caused more than seven divisions of T cells specific for each epitope, with dramatic increases in number and minor changes in hierarchy. Infections with the heterologous viruses Pichinde and vaccinia (VV) caused more than seven divisions and increases in number of T cells specific to some putatively cross-reactive but not other epitopes and resulted in substantial changes in the hierarchy of the LCMV-specific T cells. Hence, there can be memory T cell division without proliferation (i.e., increase in cell number) in the absence of Ag and division with proliferation in the presence of Ag from homologous or heterologous viruses. Heterologous protective immunity between viruses is not necessarily reciprocal, given that LCMV protects against VV but VV does not protect against LCMV. VV elicited proliferation of LCMV-induced CD8 and CD4 T cells, whereas LCMV did not elicit proliferation of VV-induced T cells. Thus, depending on the pathogen and the sequence of infection, a heterologous agent may selectively stimulate the memory pool in patterns consistent with heterologous immunity.  (+info)

Direct visualization of cross-reactive effector and memory allo-specific CD8 T cells generated in response to viral infections. (7/39)

CD8 T cell cross-reactivity between heterologous viruses has been shown to provide protective immunity, induce immunopathology, influence the immunodominance of epitope-specific T cell responses, and shape the overall memory population. Virus infections also induce cross-reactive allo-specific CTL responses. In this study, we quantified the allo-specific CD8 T cells elicited by infection of C57BL/6 (B6) mice with lymphocytic choriomeningitis virus (LCMV). Cross-reactive LCMV-specific CD8 T cells were directly visualized using LCMV peptide-charged MHC tetramers to costain T cells that were stimulated to produce intracellular IFN-gamma in response to allogeneic target cells. The cross-reactivity between T cells specific for LCMV and allogeneic Ags was broad-based, in that it involved multiple LCMV-derived peptides, but there were distinctive patterns of reactivity against allogeneic cells with different haplotypes. Experiments indicated that this cross-reactivity was not due to the expression of two TCR per cell, and that the patterns of allo-reactivity changed during sequential infection with heterologous viruses. The allo-specific CD8 T cells generated by LCMV infection were maintained at relatively high frequencies in the memory pool, indicating that memory allo-specific CD8 T cell populations can arise as a consequence of viral infections. Mice previously infected with LCMV and harboring allo-specific memory T cells were refractory to the induction of tolerance to allogeneic skin grafts.  (+info)

Attrition of virus-specific memory CD8+ T cells during reconstitution of lymphopenic environments. (8/39)

Viruses can cause a severe lymphopenia early in infection and a subsequent, lasting loss of pre-existing CD8(+) memory T cells. We therefore questioned how well virus Ag-specific memory CD8(+) T cells could reconstitute mice rendered lymphopenic as a consequence of genetics, irradiation, or viral or poly(I:C)-induced cytokines. In each case, reconstitution of the CD8(+) compartment was associated with limited division of virus-specific memory T cells and a reduction in their proportion. This indicates that foreign Ag-experienced CD44(high)CD8(+) memory T cells may respond differently to homeostatic signals than other CD44(high)CD8(+) cells, and that events inducing lymphopenia may lead to a permanent reduction in T cell memory.  (+info)

Pichinde virus (PICV) is an enveloped, negative-sense, single-stranded RNA virus that belongs to the family Arenaviridae. It is primarily found in rodents, specifically the Pichinde deer mouse (Oligoryzomys fulvescens), which are endemic to South America, particularly Colombia.

PICV is not known to cause disease in humans and is often used as a model organism for studying arenaviral pathogenesis and immunity. However, accidental laboratory infections have been reported, resulting in mild febrile illness or seroconversion without symptoms. Therefore, it is recommended that appropriate biosafety measures be taken when handling this virus.

Arenaviridae is a family of viruses that includes several species known to cause disease in humans and animals. The name "Arenaviridae" comes from the Latin word "arena," meaning "sand," due to the sandy appearance of these viruses when viewed under an electron microscope.

The virions (complete virus particles) of Arenaviridae are typically enveloped, spherical or pleomorphic in shape, and measure between 50-300 nanometers in diameter. The genome of Arenaviridae viruses is composed of two single-stranded, negative-sense RNA segments called the L (large) segment and the S (small) segment. These segments encode for several viral proteins, including the glycoprotein (GP), nucleoprotein (NP), and the RNA-dependent RNA polymerase (L).

Arenaviridae viruses are primarily transmitted to humans through contact with infected rodents or their excreta. Some of the most well-known human pathogens in this family include Lassa fever virus, Junín virus, Machupo virus, and Guanarito virus, which can cause severe hemorrhagic fevers. Other Arenaviridae viruses, such as lymphocytic choriomeningitis virus (LCMV), can cause milder illnesses in humans, including fever, rash, and meningitis.

Prevention and control of Arenaviridae infections typically involve reducing exposure to infected rodents and their excreta, as well as the development of vaccines and antiviral therapies for specific viruses in this family.

Arenaviruses, New World, are a group of viruses in the Arenaviridae family that primarily infect rodents and can cause disease in humans. They are named after the Latin word "arena" which means "sand" because of the sandy-like appearance of their virions when viewed under an electron microscope.

New World arenaviruses include several different species, such as Junín virus, Machupo virus, Guanarito virus, and Sabia virus, among others. These viruses are endemic to certain regions in the Americas, particularly in South America. They are transmitted to humans through close contact with infected rodents or their excreta, and can cause severe hemorrhagic fever with high fatality rates if left untreated.

Some New World arenaviruses, such as Junín virus and Machupo virus, have been associated with outbreaks of human disease in the past, while others, like Guanarito virus and Sabia virus, have caused sporadic cases of illness. There are currently no vaccines available for most New World arenaviruses, although research is ongoing to develop effective countermeasures against these viruses.

Hemorrhagic fever, American is a group of viral diseases that are transmitted to humans by infected ticks, mosquitoes or rodents. The most common types of American hemorrhagic fevers include:

1. Hantavirus Pulmonary Syndrome (HPS): It is caused by Sin Nombre virus and is transmitted to humans through inhalation of aerosolized urine, droppings or saliva of infected rodents.
2. Colorado Tick Fever (CTF): It is caused by a Coltivirus and is transmitted to humans through the bite of an infected tick.
3. Venezuelan Equine Encephalitis (VEE): It is caused by an Alphavirus and is transmitted to humans through the bite of an infected mosquito.
4. Eastern Equine Encephalitis (EEE) and Western Equine Encephalitis (WEE): They are also caused by Alphaviruses and are transmitted to humans through the bite of an infected mosquito.

These diseases are called hemorrhagic fevers because they are characterized by bleeding disorders, high fever, muscle and joint pain, headache, and fatigue. In severe cases, they can lead to shock, organ failure, and death. There are no specific treatments for these diseases, but early detection and supportive care can improve outcomes. Prevention measures include avoiding contact with rodents, using insect repellent, and wearing protective clothing in areas where the diseases are common.

Arenaviridae infections are viral illnesses caused by members of the Arenaviridae family of viruses, which include several Old World and New World arenaviruses. These viruses are primarily transmitted to humans through contact with infected rodents or their excreta.

Old World arenaviruses include Lassa fever virus, Lymphocytic choriomeningitis virus (LCMV), and Lujo virus, among others. They are endemic in Africa and can cause severe hemorrhagic fever with high mortality rates.

New World arenaviruses, found mainly in the Americas, include Junin virus, Machupo virus, Guanarito virus, and Sabia virus. These viruses can cause hemorrhagic fever as well, although their severity varies.

In general, Arenaviridae infections can present with a wide range of symptoms, from mild flu-like illness to severe hemorrhagic fever, depending on the specific virus and the individual's immune status. Treatment typically involves supportive care, while some viruses have specific antiviral therapies available. Prevention measures include avoiding contact with rodents and their excreta, as well as implementing public health interventions to control rodent populations in endemic areas.

**Hemorrhagic fevers, viral** are a group of severe, potentially fatal illnesses caused by viruses that affect the body's ability to regulate its blood vessels and clotting abilities. These viruses belong to several different families including *Filoviridae* (e.g., Ebola, Marburg), *Arenaviridae* (e.g., Lassa, Machupo), *Bunyaviridae* (e.g., Hantavirus, Crimean-Congo hemorrhagic fever virus) and *Flaviviridae* (e.g., Dengue, Yellow Fever).

The initial symptoms are non-specific and include sudden onset of fever, fatigue, muscle aches, joint pains, headache, and vomiting. As the disease progresses, it may lead to capillary leakage, internal and external bleeding, and multi-organ failure resulting in shock and death in severe cases.

The transmission of these viruses can occur through various means depending on the specific virus. For example, some are transmitted via contact with infected animals or their urine/feces (e.g., Hantavirus), others through insect vectors like ticks (Crimean-Congo hemorrhagic fever) or mosquitoes (Dengue, Yellow Fever), and yet others through direct contact with infected body fluids (Ebola, Marburg).

There are no specific treatments for most viral hemorrhagic fevers. However, some experimental antiviral drugs have shown promise in treating certain types of the disease. Supportive care, such as maintaining blood pressure, replacing lost fluids and electrolytes, and managing pain, is critical to improving outcomes. Prevention measures include avoiding areas where the viruses are common, using personal protective equipment when caring for infected individuals or handling potentially contaminated materials, and controlling insect vectors.

Sources: Centers for Disease Control and Prevention (CDC), World Health Organization (WHO).

RNA viruses are a type of virus that contain ribonucleic acid (RNA) as their genetic material, as opposed to deoxyribonucleic acid (DNA). RNA viruses replicate by using an enzyme called RNA-dependent RNA polymerase to transcribe and replicate their RNA genome.

There are several different groups of RNA viruses, including:

1. Negative-sense single-stranded RNA viruses: These viruses have a genome that is complementary to the mRNA and must undergo transcription to produce mRNA before translation can occur. Examples include influenza virus, measles virus, and rabies virus.
2. Positive-sense single-stranded RNA viruses: These viruses have a genome that can serve as mRNA and can be directly translated into protein after entry into the host cell. Examples include poliovirus, rhinoviruses, and coronaviruses.
3. Double-stranded RNA viruses: These viruses have a genome consisting of double-stranded RNA and use a complex replication strategy involving both transcription and reverse transcription. Examples include rotaviruses and reoviruses.

RNA viruses are known to cause a wide range of human diseases, ranging from the common cold to more severe illnesses such as hepatitis C, polio, and COVID-19. Due to their high mutation rates and ability to adapt quickly to new environments, RNA viruses can be difficult to control and treat with antiviral drugs or vaccines.

A viral RNA (ribonucleic acid) is the genetic material found in certain types of viruses, as opposed to viruses that contain DNA (deoxyribonucleic acid). These viruses are known as RNA viruses. The RNA can be single-stranded or double-stranded and can exist as several different forms, such as positive-sense, negative-sense, or ambisense RNA. Upon infecting a host cell, the viral RNA uses the host's cellular machinery to translate the genetic information into proteins, leading to the production of new virus particles and the continuation of the viral life cycle. Examples of human diseases caused by RNA viruses include influenza, COVID-19 (SARS-CoV-2), hepatitis C, and polio.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Cricetinae is a subfamily of rodents that includes hamsters, gerbils, and relatives. These small mammals are characterized by having short limbs, compact bodies, and cheek pouches for storing food. They are native to various parts of the world, particularly in Europe, Asia, and Africa. Some species are popular pets due to their small size, easy care, and friendly nature. In a medical context, understanding the biology and behavior of Cricetinae species can be important for individuals who keep them as pets or for researchers studying their physiology.

Lymphocytic choriomeningitis virus (LCMV) is an Old World arenavirus that primarily infects rodents, particularly the house mouse (Mus musculus). The virus is harbored in these mice without causing any apparent disease, but they can shed the virus in their urine, droppings, and saliva.

Humans can contract LCMV through close contact with infected rodents or their excreta, inhalation of aerosolized virus, or ingestion of contaminated food or water. In humans, LCMV infection can cause a mild to severe illness called lymphocytic choriomeningitis (LCM), which primarily affects the meninges (the membranes surrounding the brain and spinal cord) and, less frequently, the brain and spinal cord itself.

The incubation period for LCMV infection is typically 1-2 weeks, after which symptoms may appear. Initial symptoms include fever, malaise, headache, muscle aches, and nausea. In some cases, the illness may progress to involve the meninges (meningitis), resulting in neck stiffness, light sensitivity, and altered mental status. In rare instances, LCMV infection can lead to encephalitis (inflammation of the brain) or myelitis (inflammation of the spinal cord), causing more severe neurological symptoms such as seizures, paralysis, or long-term neurological damage.

Most individuals who contract LCMV recover completely within a few weeks to months; however, immunocompromised individuals are at risk for developing severe and potentially fatal complications from the infection. Pregnant women infected with LCMV may also face an increased risk of miscarriage or fetal abnormalities.

Prevention measures include avoiding contact with rodents, especially house mice, and their excreta, maintaining good hygiene, and using appropriate personal protective equipment when handling potentially contaminated materials. There is no specific treatment for LCMV infection; management typically involves supportive care to alleviate symptoms and address complications as they arise.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

An antigen is any substance that can stimulate an immune response, particularly the production of antibodies. Viral antigens are antigens that are found on or produced by viruses. They can be proteins, glycoproteins, or carbohydrates present on the surface or inside the viral particle.

Viral antigens play a crucial role in the immune system's recognition and response to viral infections. When a virus infects a host cell, it may display its antigens on the surface of the infected cell. This allows the immune system to recognize and target the infected cells for destruction, thereby limiting the spread of the virus.

Viral antigens are also important targets for vaccines. Vaccines typically work by introducing a harmless form of a viral antigen to the body, which then stimulates the production of antibodies and memory T-cells that can recognize and respond quickly and effectively to future infections with the actual virus.

It's worth noting that different types of viruses have different antigens, and these antigens can vary between strains of the same virus. This is why there are often different vaccines available for different viral diseases, and why flu vaccines need to be updated every year to account for changes in the circulating influenza virus strains.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

Arenavirus is a type of virus that belongs to the family Arenaviridae. These viruses are enveloped and have a single-stranded, bi-segmented RNA genome. They are named after the Latin word "arena" which means "sand" because their virions contain ribosomes which resemble sand granules when viewed under an electron microscope.

Arenaviruses are primarily associated with rodents and can cause chronic infection in their natural hosts. Some arenaviruses can also infect humans and other animals, causing severe hemorrhagic fevers. Examples of human diseases caused by arenaviruses include Lassa fever, Argentine hemorrhagic fever, Bolivian hemorrhagic fever, and Venezuelan hemorrhagic fever.

These viruses are typically transmitted to humans through contact with infected rodents or their excreta, but some can also be spread from person to person through close contact with an infected individual's blood or other bodily fluids. There are currently no vaccines available for most arenaviruses, and treatment is primarily supportive, focusing on managing symptoms and complications.

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