Serialin VivoPassage of HIV-1 Infection inMacaca nemestrina

Agy, Michael B.; Schmidt, Ann Marie; Florey, Mary Jo; Kennedy, Bryan; Schaefer, Greg; Katze, Michael G.; Corey, Lawrence; Morton, William R.; Bosch, Marnix L.

doi:10.1006/viro.1997.8832

Cited by 27 publications

(19 citation statements)

References 19 publications

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“…However, the rationale for using the CXCR4-tropic HIV-1 NL4-3 as an initial starting virus for in vivo studies seemed reasonable given that it has been previously shown to transiently infect pig-tailed macaques (2,3) and because the initial goal was to determine whether we could improve upon those initial results and achieve persistent infection of the pig-tail host. Clearly, further development of the model will be required for it to be useful as a model of pathogenesis or vaccine studies, but the results of the current experiments, along with those of Igarashi et al (35) and Hatziioannou et al (28), should provide guidance for future studies.…”

Section: Discussionmentioning

confidence: 99%

“…An alternative macaque species, Macaca nemestrina (pig-tailed macaque [Pt]), may be a more suitable host for HIV-1 animal model development. In contrast to other macaque species, pig-tails have been shown to support an acute, but limited, infection by HIV-1 (2,3,23,41). This greater susceptibility of Pt cells may be due to the absence of a TRIM5 isoform restricting postentry events in HIV-1 replication (13,14,63,89,91).…”

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confidence: 97%

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Vif Substitution Enables Persistent Infection of Pig-Tailed Macaques by Human Immunodeficiency Virus Type 1

Thippeshappa

Polacino

Kimata

et al. 2011

J Virol

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Among Old World monkeys, pig-tailed macaques (Pt) are uniquely susceptible to human immunodeficiency virus type 1 (HIV-1), although the infection does not persist. We demonstrate that the susceptibility of Pt T cells to HIV-1 infection is due to the absence of postentry inhibition by a TRIM5 isoform. Notably, substitution of the viral infectivity factor protein, Vif, with that from pathogenic SIVmne enabled replication of HIV-1 in Pt T cells in vitro. When inoculated into juvenile pig-tailed macaques, the Pt-tropic HIV-1 persistently replicated for more than 1.5 to 2 years, producing low but measurable plasma viral loads and persistent proviral DNA in peripheral blood mononuclear cells. It also elicited strong antibody responses. However, there was no decline in CD4؉ T cells or evidence of disease. Surprisingly, the Pt-tropic HIV-1 was rapidly controlled when inoculated into newborn Pt macaques, although it transiently rebounded after 6 months. We identified two notable differences between the Pt-tropic HIV-1 and SIVmne. First, SIV Vif does not associate with Pt-tropic HIV-1 viral particles. Second, while Pt-tropic HIV-1 degrades both Pt APOBEC3G and APOBEC3F, it prevents their inclusion in virions to a lesser extent than pathogenic SIVmne. Thus, while SIV Vif is necessary for persistent infection by Pt-tropic HIV-1, improved expression and inhibition of APOBEC3 proteins may be required for robust viral replication in vivo. Additional adaptation of the virus may also be necessary to enhance viral replication. Nevertheless, our data suggest the potential for the pig-tailed macaque to be developed as an animal model of HIV-1 infection and disease.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

Vif Substitution Enables Persistent Infection of Pig-Tailed Macaques by Human Immunodeficiency Virus Type 1

Thippeshappa

Polacino

Kimata

et al. 2011

J Virol

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“…Nevertheless, because the env genes of SIV and HIV-1 show significant sequence diversity (28), the SIV/macaque model is of limited utility for in vivo analyses of the phenotypic and immunological properties of HIV-1 envelope. Some groups have attempted to adapt HIV-1 in macaques (2,3,6,16). These efforts, however, were largely unsuccessful.…”

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confidence: 99%

Enhanced Infectivity of an R5-Tropic Simian/Human Immunodeficiency Virus Carrying Human Immunodeficiency Virus Type 1 Subtype C Envelope after Serial Passages in Pig-Tailed Macaques ( Macaca nemestrina )

Chen

Huang

Zhao

et al. 2000

J Virol

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The increasing prevalence of human immunodeficiency virus type 1 (HIV-1) subtype C infection worldwide calls for efforts to develop a relevant animal model for evaluating strategies against the transmission of the virus. A chimeric simian/human immunodeficiency virus (SHIV), SHIV CHN19 , was generated with a primary, non-syncytium-inducing HIV-1 subtype C envelope from a Chinese strain in the background of SHIV 33 . Unlike R5-tropic SHIV 162 , SHIV CHN19 was not found to replicate in rhesus CD4 ؉ T lymphocytes. SHIV CHN19 does, however, replicate in CD4 ؉ T lymphocytes of pig-tailed macaques (Macaca nemestrina). The observed replication competence of SHIV CHN19 requires the full tat/rev genes and partial gp41 region derived from SHIV 33 . To evaluate in vivo infectivity, SHIV CHN19 was intravenously inoculated, at first, into two pig-tailed and two rhesus macaques. Although all four animals became infected, the virus replicated preferentially in pig-tailed macaques with an earlier plasma viral peak and a faster seroconversion. To determine whether in vivo adaptation would enhance the infectivity of SHIV CHN19 , passages were carried out serially in three groups of two pig-tailed macaques each, via intravenous blood-bone marrow transfusion. The passages greatly enhanced the infectivity of the virus as shown by the increasingly elevated viral loads during acute infection in animals with each passage. Moreover, the doubling time of plasma virus during acute infection became much shorter in passage 4 (P4) animals (0.2 day) in comparison to P1 animals (1 to 2 days). P2 to P4 animals all became seropositive around 2 to 3 weeks postinoculation and had a decline in CD4/CD8 T-cell ratio during the early phase of infection. In P4 animals, a profound depletion of CD4 T cells in the lamina propria of the jejunum was observed. Persistent plasma viremia has been found in most of the infected animals with sustained viral loads ranging from 10 3 to 10 5 per ml up to 6 months postinfection. Serial passages did not change the viral phenotype as confirmed by the persistence of the R5 tropism of SHIV CHN19 isolated from P4 animals. In addition, the infectivity of SHIV CHN19 in rhesus peripheral blood mononuclear cells was also increased after in vivo passages. Our data indicate that SHIV CHN19 has adapted well to grow in macaque cells. This established R5-tropic SHIV CHN19 /macaque model would be very useful for HIV-1 subtype C vaccine and pathogenesis studies.

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“…[2][3][4][5][6] In fact, among nonhuman primates, only the chimpanzee, gibbon, ape, and macaque nemestrina are susceptible to HIV-1 infection, whereas no detectable replication occurs in rhesus monkey (Macaca mulatta) and cynomolgus monkey (Macaca fascicularis) peripheral blood mononuclear cells (PBMC). [7][8][9] There are several examples of intracellular restriction of retrovirus replication. Replication of murine leukemia virus (MuLV) can be blocked by a host cell factor, the product of the Fv-1 allele.…”

Section: Introductionmentioning

confidence: 99%

Infection of a Simian B Cell Line by Human and Simian Immunodeficiency Viruses

Ridolfi

Titti²,

Fulgenzi³

et al. 2004

AIDS Research and Human Retroviruses

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It is well known that HIV-1 does not establish infection in nonhuman primates, nor in cell lines derived from them, due to the existence of saturable resistance factors. In this study, we show that an in vitro established Macaca fascicularis-derived CD4(-) B cell line (F6) can be productively infected by the laboratory-adapted T-tropic HXBc2/HIV-1 strain at low multiplicity of infection, apparently because it does not express the restriction factor that has been detected in other simian cell lines. Moreover, efficient entry into F6 cells was obtained with pseudotyped recombinant HIV-1 viruses containing the laboratory-adapted T-tropic (HXBc2) or the dual-tropic (89.6) envelope glycoproteins, whereas entry of virus containing the envelope glycoproteins of the M-tropic Ba-L strain was less efficient. Virus containing primary T-tropic (Eli) envelope glycoproteins did not infect F6 cells. Furthermore, although CCR5 was not present on the cell surface and gpr15 and strl33 mRNAs were not expressed in the cells, a high level of infection of F6 cells by the M-tropic simian immunodeficiency virus SIVmac316 was observed. In contrast, F6 cells were poorly infected by T-tropic SIVmac239. Given the unique properties of the F6 cell line, i.e., that it is of simian origin yet is able to be infected by HIV-1 in a CD4-independent manner, F6 cells represent a useful model for studying cellular factors mediating resistance or permissivity to HIV-1 infection and may help to evaluate HIV-1 and SIV cell tropism.

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Serialin VivoPassage of HIV-1 Infection inMacaca nemestrina

Cited by 27 publications

References 19 publications

Vif Substitution Enables Persistent Infection of Pig-Tailed Macaques by Human Immunodeficiency Virus Type 1

Vif Substitution Enables Persistent Infection of Pig-Tailed Macaques by Human Immunodeficiency Virus Type 1

Enhanced Infectivity of an R5-Tropic Simian/Human Immunodeficiency Virus Carrying Human Immunodeficiency Virus Type 1 Subtype C Envelope after Serial Passages in Pig-Tailed Macaques ( Macaca nemestrina )

Infection of a Simian B Cell Line by Human and Simian Immunodeficiency Viruses

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