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FEMS Microbiology Reviews Sep 2019Approximately 4.4% of the human genome is comprised of endogenous retroviral sequences, a record of an evolutionary battle between man and retroviruses. Much of what we... (Review)
Review
Approximately 4.4% of the human genome is comprised of endogenous retroviral sequences, a record of an evolutionary battle between man and retroviruses. Much of what we know about viral immunity comes from studies using mouse models. Experiments using the Friend virus (FV) model have been particularly informative in defining highly complex anti-retroviral mechanisms of the intrinsic, innate and adaptive arms of immunity. FV studies have unraveled fundamental principles about how the immune system controls both acute and chronic viral infections. They led to a more complete understanding of retroviral immunity that begins with cellular sensing, production of type I interferons, and the induction of intrinsic restriction factors. Novel mechanisms have been revealed, which demonstrate that these earliest responses affect not only virus replication, but also subsequent innate and adaptive immunity. This review on FV immunity not only surveys the complex host responses to a retroviral infection from acute infection to chronicity, but also highlights the many feedback mechanisms that regulate and counter-regulate the various arms of the immune system. In addition, the discovery of molecular mechanisms of immunity in this model have led to therapeutic interventions with implications for HIV cure and vaccine development.
Topics: Adaptive Immunity; Animals; Anti-Retroviral Agents; Friend murine leukemia virus; Host Microbial Interactions; Humans; Immunity, Innate; Immunotherapy; Mice; Retroviridae Infections
PubMed: 31087035
DOI: 10.1093/femsre/fuz012 -
Poultry Science May 2018In poultry, fowl adenovirus (FAdV) and immunosuppressive virus co-infection is likely to cause decreased egg production, inclusion body hepatitis, and pericardial...
In poultry, fowl adenovirus (FAdV) and immunosuppressive virus co-infection is likely to cause decreased egg production, inclusion body hepatitis, and pericardial effusion syndrome. In this study, fowl adenovirus infection was found in parental and descendent generations of chickens. We used quantitative polymerase chain reaction (PCR) and dot blot hybridization to detect the infection of reticuloendotheliosis (REV), avian leukosis virus (ALV), and chicken infectious anemia virus (CIAV) in 480 plasma samples. The test samples were 34.58% FADV-positive, 22.29% REV-positive, 7.5% CAV-positive, and 0.63% ALV-positive. Sequence analysis showed that FADV belonged to serotype 7, which can cause inclusion body hepatitis. The ALV strain was ALV-A, in which the homology of gp85 gene and SDAU09C1 was 97.3%. The positive rate was lower because of the purification of avian leukemia, whereas the phylogenetic tree analysis of REV showed that the highest homology was with IBD-C1605, which was derived from a vaccine isolate. Through pathogen detection in poultry we present, to our knowledge, the first discovery of fowl adenovirus type 7 infection in parental chickens and found that there was co-infection of FAdV and several immunosuppressive viruses, such as the purified ALV and CIAV. This indicates that multiple infection of different viruses is ever-present, and more attention should be given in the diagnosis process.
Topics: Adenoviridae Infections; Animals; Avian Leukosis; Avian Leukosis Virus; Chicken anemia virus; Chickens; Circoviridae Infections; Coinfection; Female; Fowl adenovirus A; Phylogeny; Poultry Diseases; Reticuloendotheliosis virus; Retroviridae Infections; Tumor Virus Infections
PubMed: 29509913
DOI: 10.3382/ps/pex414 -
Human Gene Therapy Oct 2005It is of great interest to understand the molecular details of the pathways that constitute species barriers to viral infection. The tripartite motif protein TRIM5alpha... (Review)
Review
It is of great interest to understand the molecular details of the pathways that constitute species barriers to viral infection. The tripartite motif protein TRIM5alpha has emerged as an important mediator of species-specific retroviral replication and innate immunity. This review considers the role of TRIM5alpha as an antiviral protein in mammals. The methods used to identify species-specific restriction to retroviral infection, and the identification of TRIM5alpha itself, are outlined. TRIM5alpha mediates an early postentry block to sensitive retroviral infection, usually before viral DNA synthesis. Results from mutational analysis of TRIM5alpha and their contribution to a mechanistic model for TRIM5alpha antiviral activity are discussed. The antiviral role of other TRIM proteins is considered, as is the role of TRIM5alpha cytoplasmic bodies.
Topics: Animals; Antiviral Restriction Factors; Carrier Proteins; Cytoplasmic Granules; DNA Mutational Analysis; DNA, Viral; Genetic Therapy; Humans; Retroviridae; Retroviridae Infections; Species Specificity; Tripartite Motif Proteins; Ubiquitin-Protein Ligases; Virus Replication
PubMed: 16218773
DOI: 10.1089/hum.2005.16.1125 -
Veterinary Medicine and Science May 2022Retroviral infections have been reported in many species of animals, especially cattle, sheep and goats. However, there are no available reports about retrovirus...
BACKGROUND
Retroviral infections have been reported in many species of animals, especially cattle, sheep and goats. However, there are no available reports about retrovirus infection in dromedary camels. Several dromedary camels showed visible tumor-like lesions on and around the nostrils as well as around the eyes.
OBJECTIVES
Following are the objectives: to identify the causative agents of these identified tumours in dromedary camels and to perform molecular characterization of the detected strains of the causative agent.
METHODS
We extracted the nucleic acids from some fresh lesions out of these animals, and then amplified some key retrovirus genes. We amplified several regions of the rotavirus genome using the PCR technique. The obtained sequences were assembled and the phylogenetic trees were conducted per each target retrovirus gene.
RESULTS
Our results revealed a high degree of identity to some retroviruses of sheep. Phylogenetic analysis based on some retrovirus genes revealed that the causative agents of these lesions are closely related to sheep retroviruses, particularly the Jaagsiekte sheep Retrovirus (JSRV) and the ENTV.
CONCLUSIONS
To the best of our knowledge, this is the first report of retrovirus infections in dromedary camels in the Arabian Peninsula. This highlights the possible species jump for the retrovirus from sheep and goats to the dromedary camels, which live in close proximity with these animals in many parts of the world, especially the Arabian Peninsula.
Topics: Animals; Betaretrovirus; Camelus; Cattle; Cattle Diseases; Goat Diseases; Goats; Phylogeny; Retroviridae Infections; Saudi Arabia; Sheep; Sheep Diseases
PubMed: 35114072
DOI: 10.1002/vms3.760 -
PloS One 2022The effects of normal and altered intestinal microbiota on murine retroviral transmission via the gastrointestinal tract (GIT) are diverse. The role of orally...
The effects of normal and altered intestinal microbiota on murine retroviral transmission via the gastrointestinal tract (GIT) are diverse. The role of orally administered antibiotic treatment (ABX) on viral transmission, GIT microbial dysbiosis and subsequent pathogenesis of Moloney Murine Leukemia virus-temperature sensitive 1 (ts1) on BALB/c mice were studied. BALB/c mice were divided into four groups: ABXts1-Treatment/Infection;ABX-Treatment/No infection;ts1-No treatment/Infection;Ctrl (control)-No treatment/No infection. ABXts1 and ABX groups showed a significant phylogenetic shift (ANOSIM p-value = 0.001) in alpha and beta diversity comparisons for microbial community composition compared to Ctrl group. Mice in the ABXts1 and ABX groups showed megacolon compared to ts1 and Ctrl groups; ABXts1 and ts1 groups showed hepatosplenomegaly, thymus enlargement, and mesenteric lymphadenopathy compared to ABX and Ctrl groups. Ctrl group had no abnormal manifestations. ABX treatment and ts1 infection uniquely affect microbial community when compared to control: ABXts1 and ABX groups significantly reduce microbiome diversity by over 80% and ts1 group by over 30%. ABXts1 and ts1 groups' viral load and clinical manifestations of infection were comparable; antibiotic treatment did not notably affect ts1 infection. Transmission and pathophysiology of ts1 infection were not significantly altered by the microbial composition of the GI tract, but ts1 viral infection did result in microbial dysbiosis independent of antibiotic treatment.
Topics: Animals; Anti-Bacterial Agents; Female; Gastrointestinal Microbiome; Mice; Mice, Inbred BALB C; Moloney murine leukemia virus; Retroviridae Infections
PubMed: 35061714
DOI: 10.1371/journal.pone.0261689 -
Clinical Microbiology Reviews Apr 2012Xenotransplantation may be a solution to overcome the shortage of organs for the treatment of patients with organ failure, but it may be associated with the transmission... (Review)
Review
Xenotransplantation may be a solution to overcome the shortage of organs for the treatment of patients with organ failure, but it may be associated with the transmission of porcine microorganisms and the development of xenozoonoses. Whereas most microorganisms may be eliminated by pathogen-free breeding of the donor animals, porcine endogenous retroviruses (PERVs) cannot be eliminated, since these are integrated into the genomes of all pigs. Human-tropic PERV-A and -B are present in all pigs and are able to infect human cells. Infection of ecotropic PERV-C is limited to pig cells. PERVs may adapt to host cells by varying the number of LTR-binding transcription factor binding sites. Like all retroviruses, they may induce tumors and/or immunodeficiencies. To date, all experimental, preclinical, and clinical xenotransplantations using pig cells, tissues, and organs have not shown transmission of PERV. Highly sensitive and specific methods have been developed to analyze the PERV status of donor pigs and to monitor recipients for PERV infection. Strategies have been developed to prevent PERV transmission, including selection of PERV-C-negative, low-producer pigs, generation of an effective vaccine, selection of effective antiretrovirals, and generation of animals transgenic for a PERV-specific short hairpin RNA inhibiting PERV expression by RNA interference.
Topics: Animals; Animals, Genetically Modified; Endogenous Retroviruses; Humans; Retroviridae Infections; Swine; Transplantation, Heterologous
PubMed: 22491774
DOI: 10.1128/CMR.05011-11 -
Viruses Apr 2011Retroviruses cause cancers in a variety of animals and humans. Research on retroviruses has provided important insights into mechanisms of oncogenesis in humans,... (Review)
Review
Retroviruses cause cancers in a variety of animals and humans. Research on retroviruses has provided important insights into mechanisms of oncogenesis in humans, including the discovery of viral oncogenes and cellular proto-oncogenes. The subject of this review is the mechanisms by which retroviruses that do not carry oncogenes (non-acute retroviruses) cause cancers. The common theme is that these tumors result from insertional activation of cellular proto-oncogenes by integration of viral DNA. Early research on insertional activation of proto-oncogenes in virus-induced tumors is reviewed. Research on non-acute retroviruses has led to the discovery of new proto-oncogenes through searches for common insertion sites (CISs) in virus-induced tumors. Cooperation between different proto-oncogenes in development of tumors has been elucidated through the study of retrovirus-induced tumors, and retroviral infection of genetically susceptible mice (retroviral tagging) has been used to identify cellular proto-oncogenes active in specific oncogenic pathways. The pace of proto-oncogene discovery has been accelerated by technical advances including PCR cloning of viral integration sites, the availability of the mouse genome sequence, and high throughput DNA sequencing. Insertional activation has proven to be a significant risk in gene therapy trials to correct genetic defects with retroviral vectors. Studies on non-acute retroviral oncogenesis provide insight into the potential risks, and the mechanisms of oncogenesis.
Topics: Animals; Genetic Therapy; Humans; Mice; Mutagenesis, Insertional; Neoplasms; Proto-Oncogene Mas; Proto-Oncogene Proteins; Retroviridae; Retroviridae Infections; Virus Integration
PubMed: 21994739
DOI: 10.3390/v3040398 -
Viruses Jul 2023Simian retrovirus subtype 8 (SRV-8) infections have been reported in cynomolgus monkeys () in China and America, but its pathogenicity and immunogenicity are rarely...
Simian retrovirus subtype 8 (SRV-8) infections have been reported in cynomolgus monkeys () in China and America, but its pathogenicity and immunogenicity are rarely reported. In this work, the SRV-8-infected monkeys were identified from the monkeys with anemia, weight loss, and diarrhea. To clarify the impact of SRV-8 infection on cynomolgus monkeys, infected monkeys were divided into five groups according to disease progression. Hematoxylin (HE) staining and viral loads analysis showed that SRV-8 mainly persisted in the intestine and spleen, causing tissue damage. Additionally, the dynamic variations of blood routine indexes, innate and adaptive immunity, and the transcriptomic changes in peripheral blood cells were analyzed during SRV-8 infection. Compared to uninfected animals, red blood cells, hemoglobin, and white blood cells were reduced in SRV-8-infected monkeys. The percentage of immune cell populations was changed after SRV-8 infection. Furthermore, the number of hematopoietic stem cells decreased significantly during the early stages of SRV-8 infection, and returned to normal levels after antibody-mediated viral clearance. Finally, global transcriptomic analysis in PBMCs from SRV-8-infected monkeys revealed distinct gene expression profiles across different disease stages. In summary, SRV-8 infection can cause severe pathogenicity and immune disturbance in cynomolgus monkeys, and it might be responsible for fatal virus-associated immunosuppressive syndrome.
Topics: Animals; Macaca fascicularis; Retroviruses, Simian; Retroviridae Infections; Virulence; Betaretrovirus
PubMed: 37515223
DOI: 10.3390/v15071538 -
Virology Journal Nov 2017Feline leukemia virus (FeLV) is an exogenous gammaretrovirus of domestic cats (Felis catus) and some wild felids. The outcomes of FeLV infection in domestic cats vary...
BACKGROUND
Feline leukemia virus (FeLV) is an exogenous gammaretrovirus of domestic cats (Felis catus) and some wild felids. The outcomes of FeLV infection in domestic cats vary according to host susceptibility, virus strain, and infectious challenge dose. Jaguarundis (Puma yagouaroundi) are small wild felids from South and Central America. We previously reported on FeLV infections in jaguarundis. We hypothesized here that the outcomes of FeLV infection in P. yagouaroundi mimic those observed in domestic cats. The aim of this study was to investigate the population of jaguarundis at Fundação Parque Zoológico de São Paulo for natural FeLV infection and resulting outcomes.
METHODS
We investigated the jaguarundis using serological and molecular methods and monitored them for FeLV-related diseases for 5 years. We retrieved relevant biological and clinical information for the entire population of 23 jaguarundis held at zoo. Post-mortem findings from necropsies were recorded and histopathological and immunohistopathological analyses were performed. Sequencing and phylogenetic analyses were performed for FeLV-positive samples. For sample prevalence, 95% confidence intervals (CI) were calculated. Fisher's exact test was used to compare frequencies between infected and uninfected animals. P-values <0.05 were considered significant.
RESULTS
In total, we detected evidence of FeLV exposure in four out of 23 animals (17%; 95% CI 5-39%). No endogenous FeLV (enFeLV) sequences were detected. An intestinal B-cell lymphoma in one jaguarundi was not associated with FeLV. Two jaguarundis presented FeLV test results consistent with an abortive FeLV infection with seroconversion, and two other jaguarundis had results consistent with a progressive infection and potentially FeLV-associated clinical disorders and post-mortem changes. Phylogenetic analysis of env revealed the presence of FeLV-A, a common origin of the virus in both animals (100% identity) and the closest similarity to FeLV-FAIDS and FeLV-3281 (98.4% identity), originally isolated from cats in the USA.
CONCLUSIONS
We found evidence of progressive and abortive FeLV infection outcomes in jaguarundis, and domestic cats were probably the source of infection in these jaguarundis.
Topics: Animals; Animals, Zoo; Brazil; Cat Diseases; Cats; DNA, Viral; Female; Leukemia Virus, Feline; Male; Phylogeny; Polymerase Chain Reaction; Proviruses; Puma; RNA, Viral; Retroviridae Infections; Serologic Tests; Tumor Virus Infections; Viral Load
PubMed: 29149857
DOI: 10.1186/s12985-017-0889-z -
Frontiers in Immunology 2021Type I Interferons (IFNs), including numerous IFNα subtypes and IFNβ, are key molecules during innate and adaptive immune responses against viral infections. These...
Type I Interferons (IFNs), including numerous IFNα subtypes and IFNβ, are key molecules during innate and adaptive immune responses against viral infections. These cytokines exert various non-redundant biological activities, although binding to the same receptor. Persistent viral infections are often characterized by increased IFN signatures implicating a potential role of type I IFNs in disease pathogenesis. Using the well-established Friend retrovirus (FV) mouse model, we compared the therapeutic efficacy of IFNα11 and IFNβ in acute and chronic retroviral infection. We observed a strong antiviral activity of both IFNs during acute FV infection, whereas only IFNα11 and not IFNβ could also control persistent FV infection. The therapeutic treatment with IFNα11 induced the expression of antiviral IFN-stimulated genes (ISG) and improved cytotoxic T cell responses. Finally, dysfunctional CD8 T cells solely regained cytotoxicity after IFNα11 treatment. Our data provide evidence for opposing activities of type I IFNs during chronic retroviral infections. IFNβ was shown to be involved in immune dysfunction in chronic infections, whereas IFNα11 had a strong antiviral potential and reactivated exhausted T cells during persistent retroviral infection. In contrast, during acute infection, both type I IFNs were able to efficiently suppress FV replication.
Topics: Animals; Antiviral Agents; Biomarkers; Cell Line; Cytotoxicity, Immunologic; Disease Management; Disease Models, Animal; Female; Friend murine leukemia virus; Host-Pathogen Interactions; Immunologic Factors; Interferon Type I; Interferon-alpha; Interferon-beta; Leukemia Virus, Murine; Lymphocytes; Mice; Retroviridae Infections; Treatment Outcome; Viral Load; Virus Replication
PubMed: 35126368
DOI: 10.3389/fimmu.2021.809774