CMV retinitis develops in approximately 28-35% of all AIDS patients at later stages of disease, often leading to blindness. To determine whether the subset of AIDS patients who developed CMV retinitis (CMV-R) were immunologically predisposed, T cell proliferation responses to CMV were examined prospectively in an HIV infected, HLA typed, longitudinal study population. Individuals who developed CMV-R had significantly lower T cell proliferation responses to CMV, both early and late in disease, compared to CD4 matched controls who have not developed CMV-R. Since HLA proteins influence T-cell recognition, phenotypes of 21 CMV-R patients were examined to determine whether certain HLA alleles were associated with low immune response and predisposed AIDS patients to CMV-R. HLA DR7 and B44 were at increased (nearly twice the expected) frequency in those with CMV-R. The combined association of either B44, 51 or DR7 with CMV-R was highly significant (P = .008, relative risk of CMV-R = 15) with correction for multiple comparisons. Low immune responses were twice as frequent in those with (61%) compared to those without (30%) predisposing alleles. Thus, AIDS patients with immunogenetically related hyporesponsiveness to CMV antigens may be at increased risk of retinitis.

/pdf/immune-predispositions-for-cytomegalovirus-retinitis-in-aids-4i13nunizu.pdf

Immune predispositions for cytomegalovirus retinitis in AIDS. The HNRC Group.

To investigate the association of antigen specific CD4 T cell activation with HIV disease progression and AIDS-related central nervous system damage, T cell proliferation responses to HIV, CMV, and HSV were evaluated in infected individuals. CD4 T cell loss and neurocognitive impairment were assessed at 6-mo intervals. Individuals with known times of seroconversion who responded to more HIV peptides were at greater risk of progressing to < 200 CD4 T cells (P = 0.04) and dying (P = 0.03) than those with responses to fewer peptides. A positive correlation (0.52) was seen between the breadth of the HIV proliferation response and HIV plasma RNA levels. Higher proliferation responses to CMV and HSV were also associated with more rapid CD4 loss (P = 0.05). HLA phenotyped individuals (n = 150) with two HLA-DR alleles associated with response to more HIV peptides and CMV (DR-2,5,w6,10) were less likely to develop neurocognitive (P = 0.002) and neurologic impairment (P = 0.04), but were not protected from CD4 loss and death. Thus, the ability to generate a greater T cell proliferation response to HIV and opportunistic herpes viruses may lead to resistance to central nervous system damage, but also risk of more rapid HIV disease progression.

/pdf/pathogenic-and-protective-correlates-of-t-cell-proliferation-3k26s0alx5.pdf

Pathogenic and protective correlates of T cell proliferation in AIDS. HNRC Group. HIV Neurobehavioral Research Center.

CMV-specific immune responses and HLA phenotypes of AIDS patients who develop CMV retinitis

Herpes simplex virus type 2 (HSV2), a pathogen that causes genital herpes lesions, interferes with the host immune system via various known and unknown mechanisms. This virus has been used to study viral antigenic composition. Convalescent serum from HSV2-infected patients was used to identify viral antigens via 2-D protein electrophoresis and immunoblotting. The serum predominantly recognized several capsid scaffold proteins encoded by gene UL26.5, mainly ICP35. This protein has been primarily reported to function temporarily in viral assembly but is not expressed in mature virus particles. Further immunological studies suggested that this protein elicits specific antibody and cytotoxic T lymphocyte (CTL) responses in mice, but these responses do not result in a clinical protective effect in response to HSV2 challenge. The data suggested that immunodominance of ICP35 might be used to design an integrated antigen with other viral glycoproteins.

/pdf/immunological-identification-and-characterization-of-the-2nr30osgz6.pdf

Immunological Identification and Characterization of the Capsid Scaffold Protein Encoded by UL26.5 of Herpes Simplex Virus Type 2.

In this preliminary study the phenotypic distribution of HLA and DRw antigens was investigated in patients with recurrent herpes progenitalis. Ninety-three white men between the ages of 20 and 53 years, with at least a 2-year history of recurrent herpes progenitalis infection, and 558 age-matched white men from the same area of Los Angeles were studied by means of a microcytotoxicity assay. Statistical analysis of data indicated that there is no increased incidence of any HLA antigen. The B cell antigen DRw7 is present in 37% of the patients and 22% of controls, with a p value of 0.009 and a relative risk of 2.1. These results suggest that there may be genetic and immunologic factors that tend to predispose certain individuals to the development of recurrent herpes progenitalis when they are exposed to the virus.

A study of HLA and DRw antigens in severe recurrent herpes progenitalis (HS V-2) infection

In this preliminary study the phenotypic distribution of HLA and DRw antigens was investigated in patients with recurrent herpes progenitalis. Ninety-three white men between the ages of 20 and 53 years, with at least a 2-year history of recurrent herpes progenitalis infection, and 558 age-matched white men from the same area of Los Angeles were studied by means of a microcytotoxicity assay. Statistical analysis of data indicated that there is no increased incidence of any HLA antigen. The B cell antigen DRw7 is present in 37% of the patients and 22% of controls, with a p value of 0.009 and a relative risk of 2.1. These results suggest that there may be genetic and immunologic factors that tend to predispose certain individuals to the development of recurrent herpes progenitalis when they are exposed to the virus. (J AM ACAD DERMATOL 6:898-901, 1982.)

https://www.jaad.org/article/S0190-9622(82)70079-9/pdf

A study of HLA and DRw antigens in recurrent herpes progenitalis (HSV-2) infection severe

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A study of HLA and DRw antigens in severe recurrent herpes progenitalis (HS V-2) infection

A study of HLA and DRw antigens in recurrent herpes progenitalis (HSV-2) infection severe