In Vivo Replication Capacity Rather Than In Vitro Macrophage Tropism Predicts Efficiency of Vaginal Transmission of Simian Immunodeficiency Virus or Simian/Human Immunodeficiency Virus in Rhesus Macaques

Miller, Christopher J.; Marthas, Marta; Greenier, Jennifer; Liu, Ding; Dailey, Peter J.; Lu, Yichen

doi:10.1128/jvi.72.7.6277-6277.1998

Cited by 13 publications

(15 citation statements)

References 34 publications

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“…inoculation develop humoral immune responses, including neutralizing antibody (25,27), that were not observed in transiently viremic monkeys after intravaginal inoculation of SIVmac251. Third, SIVmac1A11 is not efficiently transmitted by intravaginal inoculation (29). Despite these observations, infection with an attenuated variant of SIVmac251 that is distinct from SIVmac1A11 remains a possible explanation for STV.…”

Section: Discussionmentioning

confidence: 99%

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

McChesney

Collins

Ding

et al. 1998

J Virol

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The intact cervicovaginal mucosa is a relative barrier to the sexual transmission of human immunodeficiency virus type 1 (HIV-1). In the simian immunodeficiency virus (SIV) macaque model of HIV infection, seronegative transient viremia (STV; virus isolation positive followed by repeated negative cultures) occurs after intravaginal inoculation of a low dose of pathogenicSIVmac251 (C. J. Miller, M. Marthas, J. Torten, N. Alexander, J. Moore, G. Doncel, and A. Hendrickx, J. Virol. 68:6391-6400, 1994). Thirty-one adult female macaques that had been inoculated intravaginally with pathogenic SIVmac251 became transiently viremic. One monkey that had been culture negative for a year after SIV inoculation became persistently viremic and developed simian AIDS. No other STV monkey developed persistent viremia or disease. Results of very sensitive assays showed that 6 of 31 monkeys had weak SIV-specific antibody responses. SIV-specific antibodies were not detected in the cervicovaginal secretions of 10 STV monkeys examined. Twenty of 26 monkeys had lymphocyte proliferative responses to p55 gag and/or gp130 env antigens; 3 of 6 animals, including the monkey that became persistently viremic, had detectable cytotoxic T-lymphocyte (CTL) responses to SIV. At necropsy, lymphoid tissues and vaginal mucosa were virus culture negative, but in 10 of 10 animals, SIV provirus was detected by PCR using gag-specific primer pairs. Fifty percent of the PCR-positive tissue samples were also positive for SIV gag RNA by reverse transcriptase PCR. Thus, transient viremia following intravaginal inoculation of pathogenic SIV is associated with persistent, systemic infection, either latent or very low level productive. Atypical immune responses, characterized by lymphocyte proliferation and some CTL responses in the absence of conventionally detectable antibodies, develop in transiently viremic monkeys.

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Section: Discussionmentioning

confidence: 99%

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

McChesney

Collins

Ding

et al. 1998

J Virol

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“…One hypothesis is that R5 viruses undergo selective transmission across the genital mucosa [36], where epithelial cells selectively capture R5 viruses and transfer them to CCR5‐expressing target cells [37]. A number of studies have, however, found no correlation between R5 viruses and intravaginal transmission of either simian immunodeficiency virus or simian/human immunodeficiency viruses [38,39]. Whether DCs expressing C‐type lectins such as DC‐SIGN can play a role in virus transmission across the mucosal surfaces is still unknown, but this has been postulated as a potential mechanism of infection establishment [40].…”

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confidence: 99%

Interaction of HIV‐1 with dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin‐expressing cells is influenced by gp120 envelope modifications associated with disease progression

et al. 2006

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Dendritic cells can enhance the replication of HIV‐1 in CD4+ lymphocytes through the interaction of the gp120 envelope protein with such molecules as dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin. The variable loops of gp120 have previously been shown to modulate the interaction of HIV‐1 with its principal receptor CD4 and its various coreceptors, namely CCR5 and CXCR4. Here, we utilized a panel of molecular cloned viruses to identify whether gp120 modifications can influence the virus interaction with immature dendritic cells or a cell line expressing dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin (Raji‐DC‐SIGN). The viruses encompass the R5, R5X4 and X4 phenotypes, and are based upon V1V2 and V3 sequences from a patient with disease progression. We found that dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin enhancement of virus replication can be modulated by the V1V2 length, the overall V3 charge and N‐linked glycosylation patterns; similar results were observed with immature dendritic cells. Viruses with higher V3 charges are more readily transferred to CD4+ lymphocytes when the V1V2 region is longer and contains an additional N‐linked glycosylation site, whereas transfer of viruses with lower V3 charges is greater when the V1V2 region is shorter. Viruses differing in the V1V2 and V3 regions also demonstrated differential capture by Raji‐DC‐SIGN cells in the presence of mannan. These results indicate that the interaction between HIV‐1 and immature dendritic cells via such molecules as dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin may have a role in selecting viruses undergoing transmission and evolution during disease progression.

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“…The present studies were designed to focus on the humoral responses generated during immunization and to determine the breadth of the protective response by challenging with a pathogenic simian-human immunodeficiency virus (SHIV) that contains an HIV-1-derived envelope. The challenge virus, SHIV 89.6PD , is highly infectious and causes a rapid pathology in macaques (25,28,34,40). It was constructed by using the SIV 239 molecular clone as the backbone with the substitution of the HIV-1 89.6 envelope gene for the SIV 239 envelope (35).…”

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confidence: 99%

Limited Protection from a Pathogenic Chimeric Simian-Human Immunodeficiency Virus Challenge following Immunization with Attenuated Simian Immunodeficiency Virus

Lewis

Yalley-Ogunro

Greenhouse

et al. 1999

J Virol

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Two live attenuated single-deletion mutant simian immunodeficiency virus (SIV) constructs, SIV239Δnef and SIVPBj6.6Δnef, were tested for their abilities to stimulate protective immunity in macaques. During the immunization period the animals were examined for specific immune responses and virus growth. Each construct generated high levels of specific immunity in all of the immunized animals. The SIV239Δnef construct was found to grow to high levels in all immunized animals, with some animals remaining positive for virus isolation and plasma RNA throughout the immunization period. The SIVPBj6.6Δnef was effectively controlled by all of the immunized animals, with virus mostly isolated only during the first few months following immunization and plasma RNA never detected. Following an extended period of immunization of over 80 weeks, the animals were challenged with a pathogenic simian-human immunodeficiency virus (SHIV) isolate, SIV89.6PD, by intravenous injection. All of the SIV239Δnef-immunized animals became infected with the SHIV isolate; two of five animals eventually controlled the challenge and three of five animals, which failed to check the immunizing virus, progressed to disease state before the unvaccinated controls. One of five animals immunized with SIVPBj6.6Δnef totally resisted infection by the challenge virus, while three others limited its growth and the remaining animal became persistently infected and eventually died of a pulmonary thrombus. These data indicate that vaccination with attenuated SIV can protect macaques from disease and in some cases from infection by a divergent SHIV. However, if animals are unable to control the immunizing virus, potential damage that can accelerate the disease course of a pathogenic challenge virus may occur.

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In Vivo Replication Capacity Rather Than In Vitro Macrophage Tropism Predicts Efficiency of Vaginal Transmission of Simian Immunodeficiency Virus or Simian/Human Immunodeficiency Virus in Rhesus Macaques

Cited by 13 publications

References 34 publications

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

Interaction of HIV‐1 with dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin‐expressing cells is influenced by gp120 envelope modifications associated with disease progression

Limited Protection from a Pathogenic Chimeric Simian-Human Immunodeficiency Virus Challenge following Immunization with Attenuated Simian Immunodeficiency Virus

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In Vivo Replication Capacity Rather Than In Vitro Macrophage Tropism Predicts Efficiency of Vaginal Transmission of Simian Immunodeficiency Virus or Simian/Human Immunodeficiency Virus in Rhesus Macaques

Cited by 13 publications

References 34 publications

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4+-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4+-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

Interaction of HIV‐1 with dendritic cell‐specific intercellular adhesion molecule‐3‐grabbing nonintegrin‐expressing cells is influenced by gp120 envelope modifications associated with disease progression

Limited Protection from a Pathogenic Chimeric Simian-Human Immunodeficiency Virus Challenge following Immunization with Attenuated Simian Immunodeficiency Virus

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Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV

Occult Systemic Infection and Persistent Simian Immunodeficiency Virus (SIV)-Specific CD4⁺-T-Cell Proliferative Responses in Rhesus Macaques That Were Transiently Viremic after Intravaginal Inoculation of SIV