Microsphere immunoassay for the detection of cytokines in domestic cat (Felis catus) plasma: Elevated IL-12/23 in acute feline immunodeficiency virus infections

As the hosts of lentiviruses, almost 40 species of felids (the family Felidae) are distributed around the world, and more than 20 feline species are positive for feline immunodeficiency virus (FIV), a lineage of lentiviruses. These observations suggest that FIVs globally infect a variety of feline species through multiple cross-species transmission events during million years history. Cellular restriction factors potentially inhibit lentiviral replication and limit cross-species lentiviral transmission, and cellular APOBEC3 deaminases are known as a potent restriction factor. In contrast, lentiviruses have evolutionary acquired viral infectivity factor (Vif) to neutralize APOBEC3-mediated antiviral effect. Because the APOBEC3-Vif interaction is strictly specific for viruses and their hosts, a comprehensive investigation focusing on Vif-APOBEC3 interplay can provide clues that will elucidate the roles of this virus-host interplay on cross-species transmission of lentiviruses. Here we performed a comprehensive investigation with 144 patterns of the round-robin test using 18 feline APOBEC3Z3, an antiviral APOBEC3 gene in felid, and 8 FIV Vifs and derived a matrix showing the interplay between feline APOBEC3Z3 and FIV Vif. We particularly focused on the interplay between the APOBEC3Z3 of three felids (domestic cat, ocelot and Asian golden cat) and an FIV Vif (strain Petaluma), and revealed that residues 65 and 66 of the APOBEC3Z3 protein of multiple felids are responsible for the counteraction triggered by FIV Petaluma Vif. Altogether, our findings can be a clue to elucidate not only the scenarios of the cross-species transmissions of FIVs in felids but also the evolutionary interaction between mammals and lentiviruses. Importance Most of the emergence of new virus infection is originated from the cross-species transmission of viruses. The fact that some virus infections are strictly specific for the host species indicates that certain "species barriers" in the hosts restrict cross-species jump of viruses, while viruses have evolutionary acquired their own "arms" to overcome/antagonize/neutralize these hurdles. Therefore, understanding of the molecular mechanism leading to successful cross-species viral transmission is crucial for considering the menus of the emergence of novel pathogenic viruses. In the field of retrovirology, APOBEC3-Vif interaction is a well-studied example of the battles between hosts and viruses. Here we determined the sequences of 11 novel feline APOBEC3Z3 genes and demonstrated that all 18 different feline APOBEC3Z3 proteins tested exhibit anti-FIV activity. Our comprehensive investigation focusing on the interplay between feline APOBEC3 and FIV Vif can be a clue to elucidate the scenarios of the cross-species transmissions of FIVs in felids.

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Genetically Divergent Strains of Feline Immunodeficiency Virus from the Domestic Cat (Felis catus) and the African Lion (Panthera leo) Share Usage of CD134 and CXCR4 as Entry Receptors

Journal of Virology ◽

10.1128/jvi.01312-08 ◽

2008 ◽

Vol 82 (21) ◽

pp. 10953-10958 ◽

Cited By ~ 6

Author(s):

William A. McEwan ◽

Elizabeth L. McMonagle ◽

Nicola Logan ◽

Rodrigo C. Serra ◽

Pieter Kat ◽

...

Keyword(s):

Feline Immunodeficiency Virus ◽

Felis Catus ◽

Open Reading Frames ◽

Domestic Cat ◽

Panthera Leo ◽

Cell Tropism ◽

African Lion ◽

Immunodeficiency Virus ◽

Free Ranging

ABSTRACT The env open reading frames of African lion (Panthera leo) lentivirus (feline immunodeficiency virus [FIVPle]) subtypes B and E from geographically distinct regions of Africa suggest two distinct ancestries, with FIVPle-E sharing a common ancestor with the domestic cat (Felis catus) lentivirus (FIVFca). Here we demonstrate that FIVPle-E and FIVFca share the use of CD134 (OX40) and CXCR4 as a primary receptor and coreceptor, respectively, and that both lion CD134 and CXCR4 are functional receptors for FIVPle-E. The shared usage of CD134 and CXCR4 by FIVFca and FIVPle-E may have implications for in vivo cell tropism and the pathogenicity of the E subtype among free-ranging lion populations.

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Prevalence of Feline Immunodeficiency Virus and Toxoplasma gondii in Feral Cats on St. Kitts, West Indies

Veterinary Sciences ◽

10.3390/vetsci8020016 ◽

2021 ◽

Vol 8 (2) ◽

pp. 16

Author(s):

Xinyu Chi ◽

Kexin Fang ◽

Liza Koster ◽

Jevan Christie ◽

Chaoqun Yao

Keyword(s):

Toxoplasma Gondii ◽

Feline Immunodeficiency Virus ◽

Odds Ratio ◽

Protozoan Parasite ◽

Domestic Cat ◽

Feral Cats ◽

Immunodeficiency Virus ◽

Polymerase Chain ◽

One Year

Toxoplasma gondii (T. gondii) is a cosmopolitan protozoan parasite that infects all warm-blooded species including humans. The definitive hosts of T. gondii are felid vertebrates including the domestic cat. Domestic cats shed oocysts for approximately two weeks in their feces after the primary infection. It has been shown that feline immunodeficiency virus (FIV) positive cats have a higher prevalence of and a higher titer of antibodies to T. gondii than those of FIV-negative cats. The main purposes of this study were to determine FIV prevalence and to investigate the oocysts shedding in FIV-positive and FIV-negative feral cats on St. Kitts. Fecal samples were collected from feral cats while their FIV statues were determined using a commercial SNAP kit. Total fecal DNA of each cat was tested for the presence of T. gondii DNA using a polymerase chain reaction (PCR) consistently detecting one genome equivalent. A FIV-positive status was detected in 18 of 105 (17.1%, 95% confidence interval (CI): 9.9%−24.3%) feral cats sampled. Furthermore, males were three times more likely to be FIV positive than females (p = 0.017) with an odds ratio of 3.93 (95% CI: 1.20–12.89). Adults were found to have at least twice the prevalence of FIV compared to cats younger than one year of age (p = 0.056) with an odds ratio of 3.07 (95% CI: 0.94–10.00). Toxoplasma gondii DNA was not detected in the feces of any of the 18 FIV-positive (95% CI: 0%−0.18%) and 87 FIV-negative cats (95% CI: 0%−0.04%). A follow-up study with a much bigger sample size is needed to prove or disprove the hypothesis that FIV-positive cats have a higher prevalence of shedding T. gondii oocysts than FIV-negative cats.

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Toxoplasma gondii, Dirofilaria immitis, feline immunodeficiency virus (FIV), and feline leukemia virus (FeLV) infections in stray and pet cats (Felis catus) in northwest China: co-infections and risk factors

Parasitology Research ◽

10.1007/s00436-015-4738-y ◽

2015 ◽

Vol 115 (1) ◽

pp. 217-223 ◽

Cited By ~ 18

Author(s):

Wei Cong ◽

Qing-Feng Meng ◽

Radu Blaga ◽

Isabelle Villena ◽

Xing-Quan Zhu ◽

...

Keyword(s):

Risk Factors ◽

Toxoplasma Gondii ◽

Feline Immunodeficiency Virus ◽

Dirofilaria Immitis ◽

Leukemia Virus ◽

Northwest China ◽

Felis Catus ◽

Feline Leukemia Virus ◽

Immunodeficiency Virus

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Histologic Classification and Immunophenotype of Lymphosarcomas in Cats with Naturally and Experimentally Acquired Feline Immunodeficiency Virus Infections

Veterinary Pathology ◽

10.1177/030098589603300302 ◽

1996 ◽

Vol 33 (3) ◽

pp. 264-272 ◽

Cited By ~ 75

Author(s):

J. J. Callanan ◽

B. A. Jones ◽

J. Irvine ◽

B. J. Willett ◽

I. A. P. McCandlish ◽

...

Keyword(s):

B Cell ◽

Feline Immunodeficiency Virus ◽

Cell Activation ◽

Polyclonal Antibodies ◽

Leukemia Virus ◽

Feline Leukemia Virus ◽

B Cell Activation ◽

Virus Infections ◽

Histologic Classification ◽

Immunodeficiency Virus

Lymphosarcoma (malignant lymphoma) is the commonest hematopoietic tumor in the cat. Many cases are associated with feline leukemia virus (FeLV) infection, but epidemiologic and experimental data suggest that feline immunodeficiency virus (FIV) may also have a role in lymphomagenesis. In this paper, we describe the clinical presentation, histologic classification, and immunophenotype of lymphosarcoma in eight domestic cats with natural or experimental FIV infections. The tumors were often of unusual distribution, with the majority of cases conforming to the least common anatomic classification of “miscellaneous.” Histopathologic and immunophenotypic analysis using a panel of anti-cat and cross-reactive anti-human monoclonal and polyclonal antibodies identified seven of these tumors as high-grade B cell lymphomas of the centroblastic or immunoblastic subtypes. The remaining case was a T-cell tumor associated with a concurrent FeLV infection. Our findings, together with the results of an analysis of FIV proviral DNA in these tumors, indicate that the B-cell lymphosarcomas were comparable to those observed in human and simian immunodeficiency virus infections and that the role of FIV in lymphomagenesis is indirect and related to the potential for malignant transformation during polyclonal B cell activation.

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Prevalences of feline leukaemia virus and feline immunodeficiency virus infections in cats in Sydney

Australian Veterinary Journal ◽

10.1111/j.1751-0813.1997.tb15701.x ◽

1997 ◽

Vol 75 (5) ◽

pp. 323-327 ◽

Cited By ~ 43

Author(s):

R. MALIK ◽

K. KENDALL ◽

J. CRIDLAND ◽

S. COULSTON ◽

AJ STUART ◽

...

Keyword(s):

Feline Immunodeficiency Virus ◽

Virus Infections ◽

Leukaemia Virus ◽

Immunodeficiency Virus ◽

Feline Leukaemia Virus

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Feline immunodeficiency virus dendritic cell infection and transfer

Journal of General Virology ◽

10.1099/vir.0.83068-0 ◽

2008 ◽

Vol 89 (3) ◽

pp. 709-715 ◽

Cited By ~ 4

Author(s):

Wendy S. Sprague ◽

Melissa Robbiani ◽

Paul R. Avery ◽

Kevin P. O'Halloran ◽

Edward A. Hoover

Keyword(s):

T Cells ◽

T Cell ◽

Viral Replication ◽

Feline Immunodeficiency Virus ◽

De Novo ◽

Cell Interactions ◽

Virus Infections ◽

Cell Infection ◽

Immunodeficiency Virus ◽

Viral Transfer

Feline immunodeficiency virus (FIV) interacts with dendritic cells (DC) during initiation of infection, but whether DC support or transfer FIV infection remains unclear. To address this issue, we studied the susceptibility of feline myeloid DC to FIV infection and assessed potential transfer of infection from DC to CD4+ T cells. FIV was detected in membrane-bound vesicles of DC within 2 h of inoculation, although only low concentrations of FIV DNA were found in virus-exposed isolated DC. Addition of resting CD4+ T cells increased viral DNA levels; however, addition of activated CD4+ T cells resulted in a burst of viral replication manifested by FIV p27 capsid antigen generation. To determine whether transfer of FIV infection required productively infected DC (vs virus bound to DC but not internalized), virus-exposed DC were cultured for 2 days to allow for degradation of uninternalized virus and initiation of infection in the DC, then CD4+ T blasts were added. Infection of T cells remained robust, indicating that T-cell infection is likely to be mediated by de novo viral infection of DC followed by viral transfer during normal DC/T-cell interactions. We conclude that feline DC support restricted FIV infection, which nevertheless is sufficient to efficiently transfer infection to susceptible T cells and trigger the major burst of viral replication. Feline DC/FIV/T-cell interactions (similar to those believed to occur in human immunodeficiency virus and simian immunodeficiency virus infections) highlight the means by which immunodeficiency-inducing lentiviruses exploit normal DC/T-cell interactions to transfer and amplify virus infection.

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