Disinfection and Inactivation of the Human T Lymphotropic Virus Type III/Lymphadenopathy-Associated Virus

Ls, Martin; Js, McDougal; Sl, Loskoski

doi:10.1093/infdis/152.2.400

Cited by 343 publications

(98 citation statements)

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“…8), and impaired HIV infectivity (47)(48)(49). The loss of HIV binding by DC-SIGN as the pH was lowered to 5.0 is consistent with previous reports which have shown that a drop in pH results in a conformational change in the DC-SIGN CRD that alters its binding capacity (50).…”

Section: Discussionsupporting

confidence: 89%

Surfactant Protein A Binds to HIV and Inhibits Direct Infection of CD4+ Cells, but Enhances Dendritic Cell-Mediated Viral Transfer

Gaiha

Dong

Palaniyar

et al. 2008

The Journal of Immunology

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The identification of surfactant protein A (SP-A) as an important innate immune factor of the lungs, amniotic fluid, and the vaginal tract suggests that it could play an important role during various stages of HIV disease progression and transmission. Therefore, we examined whether SP-A could bind to HIV and also had any effect on viral infectivity. Our data demonstrate that SP-A binds to HIV in a calcium-dependent manner that is inhibitable by mannose and EDTA. Affinity capture of the HIV viral lysate reveals that SP-A targets the envelope glycoprotein of HIV (gp120), which was confirmed by ELISA using recombinant gp120. Digestion of gp120 with endoglycosidase H abrogates the binding of SP-A, indicating that the high mannose structures on gp120 are the target of the collectin. Infectivity studies reveal that SP-A inhibits the infection of CD4+ T cells by two strains of HIV (BaL, IIIB) by >80%. Competition assays with CD4 and mAbs F105 and b12 suggest that SP-A inhibits infectivity by occlusion of the CD4-binding site. Studies with dendritic cells (DCs) demonstrate that SP-A enhances the binding of gp120 to DCs, the uptake of viral particles, and the transfer of virus from DCs to CD4+ T cells by >5-fold at a pH representative of the vaginal tract. Collectively, these results suggest that SP-A acts as a dual modulator of HIV infection by protecting CD4+ T cells from direct infection but enhancing the transfer of infection to CD4+ T cells mediated by DCs.

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Section: Discussionsupporting

confidence: 89%

Surfactant Protein A Binds to HIV and Inhibits Direct Infection of CD4+ Cells, but Enhances Dendritic Cell-Mediated Viral Transfer

Gaiha

Dong

Palaniyar

et al. 2008

The Journal of Immunology

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“…The inoculum was allowed to remain undisturbed for a defined period of time (15, 30, or 60 min), and then the vaginal cavity was gently lavaged with 250 ml of dilute acetic acid solution (pH 2.8) (white vinegar; Heinz Inc.). This pH has been shown to inactivate HIV (13) and SIV (C. J. Miller, unpublished data) in vitro. The volume and pH of the lavage were sufficient to inactivate and flush the inoculum from the vagina.…”

Section: Minimum Length Of Vaginal Siv Exposure Required For Mucosal mentioning

confidence: 87%

Simian Immunodeficiency Virus Rapidly Penetrates the Cervicovaginal Mucosa after Intravaginal Inoculation and Infects Intraepithelial Dendritic Cells

Gardner²,

Miller

2000

J Virol

466

372

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Despite recent insights into mucosal human immunodeficiency virus (HIV) transmission, the route used by primate lentiviruses to traverse the stratified squamous epithelium of mucosal surfaces remains undefined. To determine if dendritic cells (DC) are used by primate lentiviruses to traverse the epithelial barrier of the genital tract, rhesus macaques were intravaginally exposed to cell-free simian immunodeficiency virus SIVmac251. We examined formalin-fixed tissues and HLA-DR ؉ -enriched cell suspensions to identify the cells containing SIV RNA in the genital tract and draining lymph nodes within the first 24 h of infection. Using SIV-specific fluorescent in situ hybridization combined with immunofluorescent antibody labeling of lineagespecific cell markers, numerous SIV RNA ؉ DC were documented in cell suspensions from the vaginal epithelium 18 h after vaginal inoculation. In addition, we determined the minimum time that the SIV inoculum must remain in contact with the genital mucosa for the virus to move from the vaginal lumen into the mucosa. We now show that SIV enters the vaginal mucosa within 60 min of intravaginal exposure, infecting primarily intraepithelial DC and that SIV-infected cells are located in draining lymph nodes within 18 h of intravaginal SIV exposure. The speed with which primate lentiviruses penetrate mucosal surfaces, infect DC, and disseminate to draining lymph nodes poses a serious challenge to HIV vaccine development.

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“…Fixation of virus-infected cells in 2% PFA is widely used to allow subsequent analyses of the samples by, e.g., flow cytometry under biosafety level 1 conditions (34). Hence, we evaluated the susceptibility of XMRV to PFA inactivation.…”

Section: Resultsmentioning

confidence: 99%

Prevention of Contamination by Xenotropic Murine Leukemia Virus-Related Virus: Susceptibility to Alcohol-Based Disinfectants and Environmental Stability

Palesch

Khalid

Stürzel

et al. 2014

Appl Environ Microbiol

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Xenotropic murine leukemia virus-related virus (XMRV) represents a novel ␥-retrovirus that is capable of infecting human cells and has been classified as a biosafety level 2 (BSL-2) organism. Hence, XMRV represents a potential risk for personnel in laboratories worldwide. Here, we measured the stability of XMRV and its susceptibility to alcohol-based disinfectants. To this end, we exposed an infectious XMRV reporter virus encoding a secretable luciferase to different temperatures, pH values, and disinfectants and infected XMRV-permissive Raji B cells to measure residual viral infectivity. We found that 1 min treatment of XMRV particles at 60°C is sufficient to reduce infectivity by 99.9%. XMRV infectivity was maximal at a neutral pH but was reduced by 86% at pH 4 and 99.9% at pH 10. The common hand and surface disinfectants ethanol and isopropanol as well as the cell fixation reagent paraformaldehyde abrogated XMRV infectivity entirely, as indicated by a reduction of infectivity exceeding 99.99%. Our findings provide evidence of specific means to inactivate XMRV. Their application will help to prevent unintended XMRV contamination of cell cultures in laboratories and minimize the risk for laboratory personnel and health care workers to become infected with this biosafety level 2 organism.

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Disinfection and Inactivation of the Human T Lymphotropic Virus Type III/Lymphadenopathy-Associated Virus

Cited by 343 publications

References 0 publications

Surfactant Protein A Binds to HIV and Inhibits Direct Infection of CD4+ Cells, but Enhances Dendritic Cell-Mediated Viral Transfer

Surfactant Protein A Binds to HIV and Inhibits Direct Infection of CD4+ Cells, but Enhances Dendritic Cell-Mediated Viral Transfer

Simian Immunodeficiency Virus Rapidly Penetrates the Cervicovaginal Mucosa after Intravaginal Inoculation and Infects Intraepithelial Dendritic Cells

Prevention of Contamination by Xenotropic Murine Leukemia Virus-Related Virus: Susceptibility to Alcohol-Based Disinfectants and Environmental Stability

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