Human Immunodeficiency Virus Env-Independent Infection of Human CD4
            <sup>−</sup>
            Cells

Pang, Shen; Yu, Dawei; An, Dong Sung; Baldwin, Gayle Cocita; Xie, Yiming; Poon, Betty; Chow, Yen‐Hung; Park, No-Hee; Chen, Irvin S. Y.

doi:10.1128/jvi.74.23.10994-11000.2000

Cited by 37 publications

(52 citation statements)

References 25 publications

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“…Therefore, it is possible that CXCR4 alone can mediate FIV infection, as suggested for the Petaluma strain (26,48). However, these results might also reflect the presence of an unidentified FIV receptor on CrFK cells or nonspecific cell entry that occurred through an envelope-independent mechanism, as has been reported for HIV (14,33). In addition to CXCR4, some FIV strains were also found to interact with primate CCR3 and CCR5.…”

Section: Discussionmentioning

confidence: 50%

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Johnston

Power

2002

J Virol

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The use of chemokine receptors as cell recognition signals is a property common to several lentiviruses, including feline, human, and simian immunodeficiency viruses. Previously, two feline immunodeficiency virus (FIV) isolates, V1CSF and Petaluma, were shown to use chemokine receptors in a strain-dependent manner to infect human peripheral blood mononuclear cells (PBMC) (J. Johnston and C. Power, J. Virol. 73:2491-2498, 1999). Since the sequences of these viruses differed primarily in regions of the FIV envelope gene implicated in receptor use and cell tropism, envelope chimeras of V1CSF and Petaluma were constructed to investigate the role of envelope diversity in the profiles of chemokine receptors used by FIV to infect primate cells. By use of a receptor-blocking assay, all viruses were found to infect human and macaque PBMC through a mechanism involving the CXCR4 receptor. However, infection by viruses encoding the V3-to-V5 region of the V1CSF surface unit was also inhibited by blockade of the CCR3 or CCR5 receptor. Similar results were obtained with GHOST cells, human osteosarcoma cells expressing specific combinations of chemokine receptors. CXCR4 was required for infection by all FIV strains, but viruses expressing the V3-to-V5 region of V1CSF required the concurrent presence of either CCR3 or CCR5. In contrast, CXCR4 alone was sufficient to allow infection of GHOST cells by FIV strains possessing the V3-to-V5 region of Petaluma. To assess the role of primate chemokine receptors in productive infection, Crandell feline kidney (CrFK) cells that expressed human CXCR4, CCR3, or CCR5 in addition to feline CXCR4 were generated. Sustained infection by viruses encoding the V3-to-V5 region of V1CSF was detected in CrFK cells expressing human CCR3 or CCR5 but not in cells expressing CXCR4 alone, while all CrFK cell lines were permissive to viruses encoding the V3-to-V5 region of Petaluma. These results indicate that FIV uses chemokine receptors to infect both human and nonhuman primate cells and that the profiles of these receptors are dependent on envelope sequence, and they provide insights into the mechanism by which xenoinfections may occur.

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Section: Discussionmentioning

confidence: 50%

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Johnston

Power

2002

J Virol

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“…However, previous studies have shown that simian immunodeficiency virus (SIV) (6), HIV-2 (8,29), and some laboratory strains of HIV-1 (5,19,21) can also infect cells independent of CD4. Studies have also shown that a wide range of CD4-negative cells, including fibroblasts (36), epithelial cells (27), and neural cells (13), can be infected in vitro by certain strains of HIV. Further, it is well established that in vivo HIV can enter a wide range of cells that do not express CD4, including the cells of the nervous (12) and renal (9,28) systems.…”

Section: Human Immunodeficiency Virus Type 1 (Hiv-1) Primarily Infectmentioning

confidence: 99%

Isolation of CD4-Independent Primary Human Immunodeficiency Virus Type 1 Isolates That Are Syncytium Inducing and Acutely Cytopathic for CD8⁺Lymphocytes

Zerhouni

Nelson

Saha

2004

J Virol

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Previous studies have established the existence of CD4-independent simian immunodeficiency virus, human immunodeficiency virus type 2 (HIV-2), and laboratory strains of HIV-1. However, whether CD4-independent viruses may also exist in HIV-1-infected patients has remained unclear. We have recently reported the isolation of viruses from an AIDS patient that were able to infect CD8 ؉ cells independent of CD4, using CD8 as a receptor. Using a similar approach, here we examined viruses from 12 randomly selected patients (obtained from the AIDS Research and Reference Program, National Institutes of Health) for the presence of CD4-independent HIV-1. CD4-independent variants were isolated from infected CD8؉ cells from the viral quasispecies of 7 of 12 patients. The CD4-independent isolates were able to infect primary CD8 ؉ cells as well as a CD4؊ CD8 ؉ T-cell line. Soluble CD4 and blocking anti-CD4 or -CD8 antibody had no effect on infection of CD8 ؉ cells. Remarkably, two of the seven CD4-independent isolates, but not their parental bulk viruses, induced syncytia and caused acute death of infected CD8؉ cells. Some of the CD4-independent variants were also able to infect U87 cells that were negative for CD4, CD8, and common HIV coreceptors, suggesting a novel entry mechanism for these isolates. The CD4-independent isolates were derived from adults and children infected with subtypes A, B, and D. Although no common motif for CD4 independence was found, novel sequence changes were observed in critical areas of the envelopes of the CD4-independent viruses. These results demonstrate that HIV-1-infected patients can frequently harbor viruses that are able to mediate CD4-independent infection of CD8 ؉ cells. In addition, this study also provides evidence of primary HIV-1 variants that are syncytium inducing and acutely cytopathic for CD8 ؉ lymphocytes.

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“…Several molecules, including ICAM-1, LFA-1, MHCII, CD28, glycosaminoglycans, and glycosphingolipids, on the surface of the cell and virus have been shown to participate in HIV-1 infection, possibly by stabilizing virus-cell interactions or promoting postbinding events (3-6, 8, 9, 11-13, 32). Furthermore, HIV-1 infection independent of CD4 and chemokine receptors has been described, suggesting that novel receptors may be expressed on different cell types (2).…”

Section: Discussionmentioning

confidence: 99%

“…Although CD4, chemokines, and their receptors are clearly important in the establishment of HIV infection, there is increasing evidence that additional surface molecules act as cofactors for binding and entry. Reports of primary HIV isolates that infect cell lines lacking CD4 and chemokine receptors suggest that there are uncharacterized accessory molecules that participate in infection (2)(3)(4)(5). In addition, HIV envelope, which is acquired as the virus particle exits the cell, includes proteins and lipids that are selectively obtained from the host membrane.…”

mentioning

confidence: 99%

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

Callahan¹,

Popernack

Tsutsui³

et al. 2003

The Journal of Immunology

123

116

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HIV-1 is an enveloped retrovirus that acquires its outer membrane as the virion exits the cell. Because of the association of apoptosis with the progression of AIDS, HIV-1-infected T cells or macrophages might be expected to express elevated levels of surface phosphatidylserine (PS), a hallmark of programmed cell death. Virions produced by these cells would also be predicted to have PS on the surface of their envelopes. In this study, data are presented that support this hypothesis and suggest that PS is required for macrophage infection. The PS-specific protein annexin V was used to enrich for virus particles and to inhibit HIV-1 replication in primary macrophages, but not T cells. HIV-1 replication was also significantly inhibited with vesicles consisting of PS, but not phosphatidylcholine. PS is specifically required for HIV-1 infection because viruses pseudotyped with vesicular stomatitis virus G and amphotropic murine leukemia virus envelopes were not inhibited by PS vesicles or annexin V. These data indicate that PS is an important cofactor for HIV-1 infection of macrophages.

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Human Immunodeficiency Virus Env-Independent Infection of Human CD4 ⁻ Cells

Cited by 37 publications

References 25 publications

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Isolation of CD4-Independent Primary Human Immunodeficiency Virus Type 1 Isolates That Are Syncytium Inducing and Acutely Cytopathic for CD8⁺Lymphocytes

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

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Human Immunodeficiency Virus Env-Independent Infection of Human CD4 − Cells

Cited by 37 publications

References 25 publications

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Feline Immunodeficiency Virus Xenoinfection: the Role of Chemokine Receptors and Envelope Diversity

Isolation of CD4-Independent Primary Human Immunodeficiency Virus Type 1 Isolates That Are Syncytium Inducing and Acutely Cytopathic for CD8+Lymphocytes

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

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Product

Resources

About

Human Immunodeficiency Virus Env-Independent Infection of Human CD4 ⁻ Cells

Isolation of CD4-Independent Primary Human Immunodeficiency Virus Type 1 Isolates That Are Syncytium Inducing and Acutely Cytopathic for CD8⁺Lymphocytes