Characterization of high-risk HIV-1 seronegative hemophiliacs

Janelle R. Salkowitz; Scott F. Purvis; Howard Meyerson; Peter Zimmerman; Thomas R. O'Brien; Louis Aledort; M. Elaine Eyster; Margaret Hilgartner; Craig Kessler; Barbara A. Konkle; Gilbert C. White; James J. Goedert; Michael M. Lederman

doi:10.1006/clim.2000.4969

Characterization of high-risk HIV-1 seronegative hemophiliacs

Janelle R. Salkowitz, Scott F. Purvis, Howard Meyerson, Peter Zimmerman, Thomas R. O'Brien, Louis Aledort, M. Elaine Eyster, Margaret Hilgartner, Craig Kessler, Barbara A. Konkle, Gilbert C. White, James J. Goedert, Michael M. Lederman

Research output: Contribution to journal › Article › peer-review

53 Scopus citations

Abstract

Mechanisms that protect most high-risk HIV-1 seronegative (HRSN) persons are not well understood. Among hemophiliacs from the Multicenter Hemophilia Cohort Study who remained HIV-1 seronegative despite a high (94%) risk for acquisition of HIV-1 infection, only 7/43 were homozygous for the protective CCR5 Δ32 polymorphism. Among the remainder, neither CCR5 density nor β-chemokine production, nor in vitro susceptibility to infection with the HIV-1 isolate JR-FL could distinguish HRSN hemophiliacs from healthy controls. When compared to lymphocytes of healthy controls not at risk for HIV-1 infection, diminished spontaneous lymphocyte proliferation was seen in lymphocytes of HRSN hemophiliacs as well as in lymphocytes of hemophiliacs not at risk for HIV-1 infection. Surprisingly sera/plasmas obtained from high-risk HIV-1 seropositve hemophiliacs prior to seroconversion more often contained alloreactive antibodies than date-matched sera/plasmas obtained from HRSN hemophiliacs. Thus alloreactivity may predispose to acquisition of HIV-1 infection after parenteral exposure.

Original language	English (US)
Pages (from-to)	200-211
Number of pages	12
Journal	Clinical Immunology
Volume	98
Issue number	2
DOIs	https://doi.org/10.1006/clim.2000.4969
State	Published - 2001

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Immunology

UN SDGs

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10.1006/clim.2000.4969

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@article{2da76625fdf2497e95c1c4487f1ffa08,

title = "Characterization of high-risk HIV-1 seronegative hemophiliacs",

abstract = "Mechanisms that protect most high-risk HIV-1 seronegative (HRSN) persons are not well understood. Among hemophiliacs from the Multicenter Hemophilia Cohort Study who remained HIV-1 seronegative despite a high (94%) risk for acquisition of HIV-1 infection, only 7/43 were homozygous for the protective CCR5 Δ32 polymorphism. Among the remainder, neither CCR5 density nor β-chemokine production, nor in vitro susceptibility to infection with the HIV-1 isolate JR-FL could distinguish HRSN hemophiliacs from healthy controls. When compared to lymphocytes of healthy controls not at risk for HIV-1 infection, diminished spontaneous lymphocyte proliferation was seen in lymphocytes of HRSN hemophiliacs as well as in lymphocytes of hemophiliacs not at risk for HIV-1 infection. Surprisingly sera/plasmas obtained from high-risk HIV-1 seropositve hemophiliacs prior to seroconversion more often contained alloreactive antibodies than date-matched sera/plasmas obtained from HRSN hemophiliacs. Thus alloreactivity may predispose to acquisition of HIV-1 infection after parenteral exposure.",

author = "Salkowitz, {Janelle R.} and Purvis, {Scott F.} and Howard Meyerson and Peter Zimmerman and O'Brien, {Thomas R.} and Louis Aledort and Eyster, {M. Elaine} and Margaret Hilgartner and Craig Kessler and Konkle, {Barbara A.} and White, {Gilbert C.} and Goedert, {James J.} and Lederman, {Michael M.}",

note = "Funding Information: The authors thank Richard Koup, M.D., for his critical suggestions and Virginia Lamprecht, M.S., Barbara Kroner, Ph.D., Rick McVey, R.N., Susan Wilson, and David MacNamera for their invaluable contributions to this study. The authors would also like to thank the patients and control subjects who were kind enough to donate blood samples for analysis. This work was presented at the 39th ICAAC meeting September 26–29, 1999 San Francisco, CA, Paper 578. Informed consent was obtained from all study participants. This work was supported by the National Cancer Institute{\textquoteright}s Multicenter Hemophilia Cohort Study and by The Center for AIDS Research (CFAR) at Case Western Reserve University (AI 36219).",

year = "2001",

doi = "10.1006/clim.2000.4969",

language = "English (US)",

volume = "98",

pages = "200--211",

journal = "Clinical Immunology",

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T1 - Characterization of high-risk HIV-1 seronegative hemophiliacs

AU - Salkowitz, Janelle R.

AU - Purvis, Scott F.

AU - Meyerson, Howard

AU - Zimmerman, Peter

AU - O'Brien, Thomas R.

AU - Aledort, Louis

AU - Eyster, M. Elaine

AU - Hilgartner, Margaret

AU - Kessler, Craig

AU - Konkle, Barbara A.

AU - White, Gilbert C.

AU - Goedert, James J.

AU - Lederman, Michael M.

N1 - Funding Information: The authors thank Richard Koup, M.D., for his critical suggestions and Virginia Lamprecht, M.S., Barbara Kroner, Ph.D., Rick McVey, R.N., Susan Wilson, and David MacNamera for their invaluable contributions to this study. The authors would also like to thank the patients and control subjects who were kind enough to donate blood samples for analysis. This work was presented at the 39th ICAAC meeting September 26–29, 1999 San Francisco, CA, Paper 578. Informed consent was obtained from all study participants. This work was supported by the National Cancer Institute’s Multicenter Hemophilia Cohort Study and by The Center for AIDS Research (CFAR) at Case Western Reserve University (AI 36219).

PY - 2001

Y1 - 2001

N2 - Mechanisms that protect most high-risk HIV-1 seronegative (HRSN) persons are not well understood. Among hemophiliacs from the Multicenter Hemophilia Cohort Study who remained HIV-1 seronegative despite a high (94%) risk for acquisition of HIV-1 infection, only 7/43 were homozygous for the protective CCR5 Δ32 polymorphism. Among the remainder, neither CCR5 density nor β-chemokine production, nor in vitro susceptibility to infection with the HIV-1 isolate JR-FL could distinguish HRSN hemophiliacs from healthy controls. When compared to lymphocytes of healthy controls not at risk for HIV-1 infection, diminished spontaneous lymphocyte proliferation was seen in lymphocytes of HRSN hemophiliacs as well as in lymphocytes of hemophiliacs not at risk for HIV-1 infection. Surprisingly sera/plasmas obtained from high-risk HIV-1 seropositve hemophiliacs prior to seroconversion more often contained alloreactive antibodies than date-matched sera/plasmas obtained from HRSN hemophiliacs. Thus alloreactivity may predispose to acquisition of HIV-1 infection after parenteral exposure.

AB - Mechanisms that protect most high-risk HIV-1 seronegative (HRSN) persons are not well understood. Among hemophiliacs from the Multicenter Hemophilia Cohort Study who remained HIV-1 seronegative despite a high (94%) risk for acquisition of HIV-1 infection, only 7/43 were homozygous for the protective CCR5 Δ32 polymorphism. Among the remainder, neither CCR5 density nor β-chemokine production, nor in vitro susceptibility to infection with the HIV-1 isolate JR-FL could distinguish HRSN hemophiliacs from healthy controls. When compared to lymphocytes of healthy controls not at risk for HIV-1 infection, diminished spontaneous lymphocyte proliferation was seen in lymphocytes of HRSN hemophiliacs as well as in lymphocytes of hemophiliacs not at risk for HIV-1 infection. Surprisingly sera/plasmas obtained from high-risk HIV-1 seropositve hemophiliacs prior to seroconversion more often contained alloreactive antibodies than date-matched sera/plasmas obtained from HRSN hemophiliacs. Thus alloreactivity may predispose to acquisition of HIV-1 infection after parenteral exposure.

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JO - Clinical Immunology

JF - Clinical Immunology

IS - 2

ER -

Characterization of high-risk HIV-1 seronegative hemophiliacs

Abstract

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