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Thirty-five homosexual men who had been the regular sexual partners (for at least 6 months) of anti-HIV-positive patients with AIDS (N = 18) or PGL (N = 17) were studied. Twenty-one (60%) were seropositive, but 14 (40%) were consistently anti-HIV-negative. The duration of relationship with the index case was not statistically different in seropositive compared to seronegative partners; median 26 months (range 7-60) vs 30 months (range 7-60). However, seropositive partners had a significantly higher monthly number of other sexual partners and sexually transmitted diseases and a higher frequency of insertive and receptive anal intercourse in the preceding five years. The risk of acquiring HIV infection was significantly increased by frequent receptive anal intercourse when the frequency of insertive was controlled for but not the converse. Seronegative partners had undetectable antibodies by live and fixed cell immunofluorescence and by radioimmunoprecipitation and were repeatedly negative by competitive enzyme immunoassay. Furthermore, the sera of seronegative partners lacked HIV neutralising activity. Peripheral blood mononuclear cells (PBMCs) from seronegative partners, stained with monoclonal antibodies to seven different CD4 epitopes, revealed no differences when compared to those from heterosexual controls and no qualitative differences from cells from seropositive individuals. In addition, PBMCs from seronegative partners could be productively infected by HIV in vitro. If resistance to infection in seronegative partners exists, then it is likely that mechanisms other than a specific humoral immunity or CD4 polymorphisms are involved.
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
August 1988,
The Medical journal of Australia,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
May 1984,
Lancet (London, England),
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
August 1987,
Scottish medical journal,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
March 1989,
American journal of epidemiology,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
March 1989,
Journal of clinical immunology,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
May 1985,
Annals of internal medicine,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
March 1992,
The Journal of the American Osteopathic Association,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
August 1988,
American journal of public health,
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
July 2001,
Internal medicine (Tokyo, Japan),
I V Weller, and
C A Carne, and
Q Sattentau, and
A Smith, and
R S Tedder, and
P Clapham, and
A Dalgleish, and
J Weber, and
M W Adler
October 1987,
The New England journal of medicine,
