Feline lentivirus infection in nondomestic felids.
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Feline immunodeficiency virus
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Feline immunodeficiency virus
Viremia
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Feline immunodeficiency virus
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Feline immunodeficiency virus
Group-specific antigen
Medical microbiology
Immunodeficiency Syndrome
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Feline immunodeficiency virus
Medical microbiology
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Infection of domestic cats with feline immunodeficiency virus (FIV) causes progressive immunological deterioration similar to that caused by human immunodeficiency virus (HIV). Lentiviruses related to but phylogenetically distinct from FIV have been detected in several non-domestic feline species. Serological cross-reactivity of these viruses raises the question as to whether inter-species transmission may occur. To address this issue, we asked whether lion lentivirus (FIV-Ple) or two strains of puma lentivirus (FIV-Pco) could replicate or cause disease in domestic cats. We found that domestic cats inoculated with FIV-Ple developed persistent cell-associated viraemia, transient cell-free viraemia and antiviral antibody. Clinical disease was not detected throughout a 6 month observation period. Two of four cats inoculated with FIV-Pco developed cell-associated viraemia, seroconverted and exhibited transient lymphadenopathy. No changes in white blood cell parameters or other haematological abnormalities were detected in any of the infected cats. Virus-specific RNA was detected in cocultivated lymphocytes of all infected cats by RT- PCR. These findings reveal that non-domestic cat lentiviruses are infectious for domestic cats and can establish persistent infection in the absence of disease.
Infectivity
Puma
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Medical microbiology
Feline immunodeficiency virus
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A more or less pronounced resistance to superinfection by a second strain of the infecting virus has been observed in many lentivirus-infected hosts. We used a chimeric feline immunodeficiency virus (FIV), designated FIVchi, containing a large part of the env gene of a clade B virus (strain M2) and all the rest of the genome of a clade A virus (a p34TF10 molecular clone of the Petaluma strain modified to grow in lymphoid cells), to gain insights into such resistance. FIVchi was infectious and moderately pathogenic for cats and in vitro exhibited the neutralization specificity of the env donor. The experiments performed were bidirectional, in that cats preinfected with either parental virus were challenged with FIVchi and vice versa. The preinfected animals were partially or completely protected relative to what was observed in naïve control animals, most likely due, at least in part, to the circumstance that in all the preinfecting/challenge virus combinations examined, the first and the second virus shared significant viral components. Based on the proportions of complete protection observed, the role of a strongly matched viral envelope appeared to be modest and possibly dependent on the time interval between the first and the second infection. Furthermore, complete protection and the presence of measurable neutralizing antibodies capable of blocking the second virus in vitro were not associated.
Superinfection
Feline immunodeficiency virus
Strain (injury)
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Feline immunodeficiency virus
Group-specific antigen
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The ability of feline immunodeficiency virus (FIV) isolates from subtypes A and B to superinfect cats and cell cultures was tested. Three specific pathogen-free (SPF) cats were first inoculated with 10 ID50 of subtype B virus (FIVBang) and 30 weeks later inoculated with 100ID50 of subtype A virus (FIVPet). On the basis of subtype-specific PCR analysis, both FIV subtypes were detected in the peripheral blood lymphocytes (PBLs) of two of three cats from 9 to 30 weeks following the second inoculation. Only the first virus was detected in the bone marrow (BM) cells of these two cats until 30 weeks following the second inoculation, at which time the second virus was finally detected in their BM cells. Both cats developed significant virus-neutralizing (VN) antibodies to the second virus by 15 weeks following the second inoculation; but only one cat had high VN titers to the first virus, which remained at the same level even after the second inoculation. The two control cats inoculated with only the second virus developed VN titers specifically to the second virus and were consistently PCR positive for the virus in PBLs and BM cells starting 9 weeks postinoculation. Thus a delay in BM infection with the second virus was observed in the two superinfected cats. In contrast, one of three cats had neither VN antibodies to the second virus nor PCR signal of the second virus in its PBLs, BM, and lymph node throughout the 30 weeks of study and it appeared to be resistant to superinfection. However, this cat had high constant levels of both the first virus and VN antibodies to the first virus. In the in vitro superinfection studies, both FIVPet and FIVBang were detected in the primary PBL cultures after either simultaneous coinfection or superinfection (second virus infected 1 week later) and in the FIVPet-producer cell line after superinfection with FIVBang. Thus our in vitro results support our in vivo findings, which suggest that at a certain stage of initial FIV infection infected cats can be superinfected with another FIV subtype. These findings present the complexity of the FIV immunopathogenicity during multiple FIV exposure and shed some concern as to whether an FIV vaccine developed from a single subtype can completely protect cats against infection with other FIV subtypes. As a small animal AIDS model, our findings should also provide some insight into the events that occur during multiple HIV exposure in humans and in identifying approaches for HIV vaccine development.
Superinfection
Feline immunodeficiency virus
Specific-pathogen-free
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The antibody response in cats to feline immunodeficiency virus (FIV) reverse transcriptase (RT) was followed for 3 years. Eight of the nine cats used in this study produced reverse transcriptase-inhibiting (RTI) antibodies. Relative inhibitory means of 2.9%, 18.4%, 33%, and 47% were found 6, 12, 24, and 36 months, respectively, after infection with FIV. The enzyme activity was suppressed by ≥78% with the use of 100 μg of FIV-associated IgG. The RTI antibodies were FIV-specific, as they did not inhibit other mammalian retroviral polymerases, including feline leukemia virus RT. An RT-inhibition assay with sera in the presence of protein A and immunoblot analysis showed that antibody binding to FIV RT protein p62 is independent of antibody ability to block enzyme activity. Viral RT released by detergent-treated virus was stable for more than 6 weeks at 4°C, whereas its activity was reduced by 50% after 2 weeks at 37°C. Because significant concentrations of RTI antibodies are detected only at 1 to 2 years after infection, they can be used to determine the approximate time of virus infection and as a marker for disease progression.
Feline immunodeficiency virus
Feline leukemia virus
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