Feline immunodeficiency virus env gene evolution in experimentally infected cats

Kraase, Martin; Sloan, Richard D.; Klein, Dieter; Logan, Nicola; McMonagle, Linda; Biek, Roman; Willett, Brian J.; Hosie, Margaret J.

doi:10.1016/j.vetimm.2009.10.015

Cited by 19 publications

(28 citation statements)

References 55 publications

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“…The presence of identical amplicons in cats at three different sampling times suggest that factors which tend to generate false diversity (polymerase template switching, PCR-induced errors) did not affect our results. Furthermore, the results presented here are in agreement with previous FIV studies employing ‘bulk’ PCR (Ikeda et al , 2004; Motokawa et al , 2005), end-point dilution proviral DNA PCR (Kraase et al , 2010) as well as a study examining sequences from plasma viral RNA (Huisman et al , 2008), and we observed low sequence variation and high genetic stability of FIV in a relatively large sample of naturally infected cats.…”

Section: Discussionsupporting

confidence: 92%

Rapid evolution of the env gene leader sequence in cats naturally infected with feline immunodeficiency virus

Bęczkowski

Hughes

Biek

et al. 2015

Journal of General Virology

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Analysing the evolution of feline immunodeficiency virus (FIV) at the intra-host level is important in order to address whether the diversity and composition of viral quasispecies affect disease progression. We examined the intra-host diversity and the evolutionary rates of the entire env and structural fragments of the env sequences obtained from sequential blood samples in 43 naturally infected domestic cats that displayed different clinical outcomes. We observed in the majority of cats that FIV env showed very low levels of intra-host diversity. We estimated that env evolved at a rate of 1.16×10−3 substitutions per site per year and demonstrated that recombinant sequences evolved faster than non-recombinant sequences. It was evident that the V3–V5 fragment of FIV env displayed higher evolutionary rates in healthy cats than in those with terminal illness. Our study provided the first evidence that the leader sequence of env, rather than the V3–V5 sequence, had the highest intra-host diversity and the highest evolutionary rate of all env fragments, consistent with this region being under a strong selective pressure for genetic variation. Overall, FIV env displayed relatively low intra-host diversity and evolved slowly in naturally infected cats. The maximum evolutionary rate was observed in the leader sequence of env. Although genetic stability is not necessarily a prerequisite for clinical stability, the higher genetic stability of FIV compared with human immunodeficiency virus might explain why many naturally infected cats do not progress rapidly to AIDS.

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Section: Discussionsupporting

confidence: 92%

Rapid evolution of the env gene leader sequence in cats naturally infected with feline immunodeficiency virus

Bęczkowski

Hughes

Biek

et al. 2015

Journal of General Virology

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“…We have investigated the primary isolate of FIV Petaluma that had been maintained solely in peripheral blood mononuclear cells and have identified CD134-independent variants among the viral quasispecies (data not shown). Combined with our own observations in which CD134-independent strains of FIV arose in vivo following infection with the CD134-dependent GL8 strain of FIV (23), it would appear that there is selective pressure in vivo for the generation of CD134-independent strains of virus. We have shown previously that the humoral immune response can exert a selective pressure that is capable of modulating the virus-receptor interaction (64).…”

Section: Discussionmentioning

confidence: 68%

Feline Tetherin Efficiently Restricts Release of Feline Immunodeficiency Virus but Not Spreading of Infection

Dietrich

McMonagle

Petit

et al. 2011

J Virol

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Innate resistance to retroviral infection and replication is induced by interferons (IFNs). IFN-inducible factors restricting viral replication include the cytidine deaminase APOBEC3G (40, 60) and the E3 ubiquitin ligase TRIM5 (1), both of which target replication primarily during the process of viral entry. A third IFN-inducible activity, tetherin (BST-2/ CD317/HM1.24), acts to restrict viral release (13,35,36,41,62). The importance of these factors in controlling viral replication is underlined by the requirement for lentiviral genomes to encode trans-acting countermeasures; lentiviral Vif proteins (33,54,55) and spumaviral Bet proteins (28, 42, 51) counteract APOBECs whereas HIV-1 Vpu, HIV-2 Nef, and HIV-2 and simian immunodeficiency virus (SIV) Envs may counteract tetherins (15,18,26,35,36,62,65).Tetherin is a type II single-pass transmembrane protein. It is anchored to the cell membrane by both N-terminal transmembrane domain and C-terminal glycophosphatidylinositol (GPI) anchors that are linked by an extracellular coiled-coil domain that promotes dimerization of adjacent tetherin molecules. Accordingly, tetherin in both the cell membrane and the envelope of the budding virus can prevent virion release either by direct cross-linking or by the formation of dimers between adjacent coiled-coil domains (41). The primary role for tetherin remains unclear; however, it is likely that, by trapping enveloped viruses at the cell surface, tetherin prevents the further dissemination of nascent virions. However, given the constitutive high-level expression of tetherin on plasmacytoid dendritic cells (pDC [type I IFN-producing cells]) (5), tetherin may play a more fundamental role in the initiation and perpetuation of a virus-specific immune response (58).The domestic cat lineage has faced multiple invasions by viruses from the family Retroviridae. In addition to an exogenous gammaretrovirus (feline leukemia virus [FeLV]), a lentivirus (feline immunodeficiency virus [FIV]), and a spumavirus (feline foamy virus [FFV]), cats also harbor the endogenous RD114 gamma retrovirus (47, 48) and full-length endogenous FeLVs (50). While lentiviruses have spread throughout the Felidae, from lions in Africa to pumas in North America and Pallas cats in Mongolia (61), the gamma retroviruses are restricted solely to domestic cats (3,4,47,48), although occasional cross-species transmission events have been recorded in Florida panthers (37) and Iberian lynxes (30). The limited distribution of the gamma retroviruses among felids suggests that they entered the domestic cat population after the divergence of the Felis lineage from the other felids circa 6.2 million years ago (19). The presence of three exogenous members and one endogenous member of the Retroviridae in domestic cats offers an intriguing insight into the retrovirus-host interaction. As cats express a truncated TRIM5 lacking a capsid-binding B30.2/SPRY domain (29), their ability to suppress retroviral replication may be impaired. If tetherin is to have a major role in the contro...

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“…McDonnel et al reviewed FIV latency and the strengths of the FIV-infected cat as a model of the HIV-infected human [61]. Different cohorts of naturally and experimentally infected cats have demonstrated either undetectable or consistently detectable plasma viraemia during the asymptomatic phase, which may be due to differences in viral strains, inoculating dose, age of the animal or other factors [7,84,98,104,[115][116][117][118]. The cellular mechanisms involved in FIV latency have been identified in both in vitro and in vivo infection systems [52,84,[119][120][121][122].…”

Section: Fiv Latencymentioning

confidence: 99%

Central and peripheral reservoirs of feline immunodeficiency virus in cats: a review

Eckstrand

Sparger

Murphy

2017

Journal of General Virology

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Infection with feline immunodeficiency virus (FIV), a lentivirus similar to human immunodeficiency virus (HIV), results in lifelong viral persistence and progressive immunopathology in the cat. FIV has the ability to infect and produce infectious virus in a number of different cell types. FIV provirus can also be maintained in a replication-competent but transcriptionally quiescent state, facilitating viral persistence over time. Immediately after the initial infection, FIV infection quickly disseminates to many anatomical compartments within the host including lymphoid organs, gastrointestinal tract and brain. Collectively, the anatomic and cellular compartments that harbour FIV provirus constitute the viral reservoir and contain foci of both ongoing viral replication and transcriptionally restricted virus that may persist over time. The relative importance of the different phenotypes observed for infected cells, anatomic compartment, replication status and size of the reservoir represent crucial areas of investigation for developing effective viral suppression and eradication therapies. In this review, we discuss what is currently known about FIV reservoirs, and emphasize the utility of the FIV-infected cat as a model for the HIV-infected human.

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Feline immunodeficiency virus env gene evolution in experimentally infected cats

Cited by 19 publications

References 55 publications

Rapid evolution of the env gene leader sequence in cats naturally infected with feline immunodeficiency virus

Rapid evolution of the env gene leader sequence in cats naturally infected with feline immunodeficiency virus

Feline Tetherin Efficiently Restricts Release of Feline Immunodeficiency Virus but Not Spreading of Infection

Central and peripheral reservoirs of feline immunodeficiency virus in cats: a review

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