Determinants of disease in the simian immunodeficiency virus-infected rhesus macaque: characterizing animals with low antibody responses and rapid progression.

Dykhuizen, Marta; Mitchen, Jacque; Montefiori, David C.; Thomson, James A.; Acker, L; Lardy, H; Pauza, C. David

doi:10.1099/0022-1317-79-10-2461

Cited by 59 publications

(60 citation statements)

References 21 publications

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“…14,[18][19][20] Rapid disease progression with lymphoid depletion more analogous to FIV-C disease has been described in SIV-infected macaques, which succumb to AIDS after a few months (versus weeks) of infection. 15,38,52 Although there have been occasional reports of individual cats developing rapid disease following FIV infection, 9,49,54 prior to FIV-C transmission studies this response was rare. As with SIVsmmPBj14 infection, 64 rapid FIV-C disease occurred less frequently after mucosal than after intravenous infection.…”

Section: Discussionmentioning

confidence: 99%

“…One-day-old kittens (n ϭ 14; cat Nos. [10][11][12][13][14][15][16][17][18][19][37][38][39][40] were inoculated via the oral and nasal mucosae with 200 l of 200 TCID 50 /ml (50% tissue culture infective dose; n ϭ 6) cell-free infectious plasma or 300 TCID 50 /ml (n ϭ 8) cellfree infectious culture. Similarly, 8-week-old cats were inoculated via the oral and nasal mucosae (n ϭ 6; cat Nos.…”

Section: Animals and Sample Collectionmentioning

confidence: 99%

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Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Obert

Hoover

2000

Vet Pathol

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Abstract. Feline immunodeficiency virus (FIV) infection typically has a prolonged and variable disease course in cats, which can limit its usefulness as a model for human immunodeficiency virus infection. A clade C FIV isolate (FIV-C) has been associated with high viral burdens and rapidly progressive disease in cats. FIV-C was transmissible via oral-nasal, vaginal, or rectal mucosal exposure, and infection resulted in one of three disease courses: rapid, conventional/slow, or regressive. The severity of the pathologic changes paralleled the disease course. Thymic depletion was an early lesion and was correlated with detection of FIV RNA in thymocytes by in situ hybridization. The major changes in thymic cell populations were depletion of p55ϩ/S100ϩ dendritic cells, CD3Ϫ cells, CD4ϩ/CD8Ϫ cells, and CD4ϩ/CD8ϩ cells and increases in apoptosis, CD45Rϩ B cells, and lymphoid follicles. In contrast to thymic depletion, peripheral lymphoid tissues often were hyperplastic. Mucosally transmitted FIV-C is thymotropic and induces a spectrum of lymphoid lesions and disease mirroring that seen with the human and simian immunodeficiency virus infections.

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Section: Discussionmentioning

confidence: 99%

Section: Animals and Sample Collectionmentioning

confidence: 99%

Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Obert

Hoover

2000

Vet Pathol

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“…36 CD4 þ T-cell counts turned out to be an inadequate marker for the diagnosis of AIDS since many rapid progressors still had increasing CD4 þ counts by the time of euthanasia. 36,51,52 Viral RNA copy number could not be used as a proxy for AIDS as many monkeys were infected at a time when RNA copy number was not routinely analyzed. However, for most monkeys cellassociated viral load data were available.…”

Section: Diagnosis Of Aids-like Diseasementioning

confidence: 99%

Mhc class I haplotypes associated with survival time in simian immunodeficiency virus (SIV)-infected rhesus macaques

Sauermann

Siddiqui

et al. 2007

Genes Immun

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In both human immunodeficiency virus-infected humans and simian immunodeficiency virus (SIV)-infected macaques, genes encoded in the major histocompatibility complex (MHC) class I region are important determinants of disease progression. However, compared to the human human lymphocyte antigen complex, the macaque MHC region encodes many more class I genes. Macaques with the same immunodominant class I genes express additional Mhc genes with the potential to influence the disease course. We therefore assessed the association between of the Mhc class I haplotypes, rather than single gene variants, and survival time in SIV-infected rhesus macaques (Macaca mulatta). DNA sequence analysis and Mhc genotyping of 245 pedigreed monkeys identified 17 Mhc class I haplotypes that constitute 10 major genotypes. Among 81 vaccination-naive, SIV-infected macaques, 71 monkeys carried at least one Mhc class I haplotype encoding only MHC antigens that were incapable of inducing an effective anti-SIV cytotoxic T lymphocytes response. Study of these macaques enabled us to relate individual Mhc class I haplotypes to slow, medium and rapid disease progression. In a post hoc analysis, classification according to disease progression was found to explain at least 48% of the observed variation of survival time.

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“…1D-G). On the other hand, the number of cells that were CD3 -CD8 + , also recognized as the phenotype for NK cells (Dykhuizen et al 1998(Dykhuizen et al , 2000, increased slightly during the first day after infection, though the absolute numbers then decreased consistently in all the monkeys tested > 2 days after inoculation (Fig. 1H).…”

Section: Viremia Was Detected 4-6 Days After Inoculation With Lcmv-we -mentioning

confidence: 99%

Circulating natural killer and γδ T cells decrease soon after infection of rhesus macaques with lymphocytic choriomeningitis virus

Rodas

Cairo

Djavani

et al. 2009

Mem. Inst. Oswaldo Cruz

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Rhesus macaques infected with the WE strain of lymphocytic choriomeningitis virus (LCMV-WE) serve as a model for human infection with Lassa fever virus. To identify the earliest events of acute infection, rhesus macaques were monitored immediately after lethal infection for changes in peripheral blood mononuclear cells (PBMCs). Changes in CD3, CD4, CD8 and CD20 subsets did not vary outside the normal fluctuations of these blood cell populations; however, natural killer (NK) and γδ T cells increased slightly on day 1 and then decreased significantly after two days. The NK subsets responsible for the decrease were primarily CD3 -CD8 + or CD3 -CD16 + and not the NKT (primarily CD3 + CD56 + ) subset. Macaques infected with a non-virulent arenavirus, LCMV-Armstrong, showed a similar drop in circulating NK and γδ T cells, indicating that this is not a pathogenic event. Vγ9 T cells, representing the majority of circulating γδ T cells in rhesus macaques, displayed significant apoptosis when incubated with LCMV in cell culture; however, the low amount of cell death for virus-co-cultured NK cells was insufficient to account for the observed disappearance of this subset. Our observations in primates are similar to those seen in LCMV-infected mice, where decreased circulating NK cells were attributed to margination and cell death. Thus, the disappearance of these cells during acute hemorrhagic fever in rhesus macaques may be a cytokine-induced lymphopenia common to many virus infections. Keywords: NK cells -γδ T -rhesus macaque -LCMV -hemorrhagic feverArenaviruses are rodent-borne pathogens that have occasionally been known to cause lethal diseases in human beings (Oldstone 2002, Salvato & Rodas 2005. Every year, Lassa fever and the South American hemorrhagic fever viruses account for almost half a million cases worldwide, with approximately 16% mortality (Jahrling et al. 1985, McCormick et al. 1986, Fisher-Hoch et al. 2000. Although rodents serve as a reservoir for arenaviruses, studies of hemorrhagic fever have relied on guinea pig, hamster and primate models rather than mouse models because the disease mechanism is fundamentally different in non-reservoir species (Peters et al. 1987).Numerous murine studies of viral persistence and cell-mediated immunity have involved the prototype arenavirus, lymphocytic choriomeningitis virus (LCMV) , Ahmed et al. 1984, Salvato et al. 1991. The WE strain of LCMV is hepatotropic in mice, guinea pigs and primates (Riviere et al. 1985, Zinkernagel et al. 1986, Lukashevich et al. 2002, but in contrast to murine LCMV infections, LCMV-WE infection of rhesus macaques can resemble Lassa hemorrhagic fever in human beings (Jahrling et al. 1980, Peters et al. 1987, Lukashevich et al. 2002. The Armstrong (ARM) strain of LCMV does not cause overt disease in monkeys, even after intravenous inoculation (Danes et al. 1963, Peters et al. 1987, Lukashevich et al. 2002.Several immunological studies have shown the importance of CD8 T lymphocytes in both protection and in induction of immuno-pathogenesis i...

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Determinants of disease in the simian immunodeficiency virus-infected rhesus macaque: characterizing animals with low antibody responses and rapid progression.

Cited by 59 publications

References 21 publications

Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Relationship of Lymphoid Lesions to Disease Course in Mucosal Feline Immunodeficiency Virus Type C Infection

Mhc class I haplotypes associated with survival time in simian immunodeficiency virus (SIV)-infected rhesus macaques

Circulating natural killer and γδ T cells decrease soon after infection of rhesus macaques with lymphocytic choriomeningitis virus

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