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In both human immunodeficiency virus-infected humans and simian immunodeficiency virus (SIV)-infected macaques, genes encoded in the major histocompatibility complex (MHC) class I region are important determinants of disease progression. However, compared to the human human lymphocyte antigen complex, the macaque MHC region encodes many more class I genes. Macaques with the same immunodominant class I genes express additional Mhc genes with the potential to influence the disease course. We therefore assessed the association between of the Mhc class I haplotypes, rather than single gene variants, and survival time in SIV-infected rhesus macaques (Macaca mulatta). DNA sequence analysis and Mhc genotyping of 245 pedigreed monkeys identified 17 Mhc class I haplotypes that constitute 10 major genotypes. Among 81 vaccination-naive, SIV-infected macaques, 71 monkeys carried at least one Mhc class I haplotype encoding only MHC antigens that were incapable of inducing an effective anti-SIV cytotoxic T lymphocytes response. Study of these macaques enabled us to relate individual Mhc class I haplotypes to slow, medium and rapid disease progression. In a post hoc analysis, classification according to disease progression was found to explain at least 48% of the observed variation of survival time.

Trials in approximately 3,900 adults were conducted with influenza A/New Jersey/76, A/Victoria/75, and B/Hong Kong/72 virus vaccines. Subjects were observed following a standard protocol, and serologic testing was performed in a single laboratory. The data indicate that prior experience of the population with earlier influenza viruses ("priming") is a determinant in response to vaccination. Thus, participants older than 25 years showed good serologic response following a single inoculation of A/New Jersey/76 virus, while younger persons responded poorly. Serological responses to A/Victoria/75 and B/Hong Kong/72 viruses were, in contrast, equally good in the younger and older adults. Whole-virus vaccines were measurably more reactive than split-virus vaccines, a finding more easily discernined in unprimed populations. In the unprimed persons, a single dose of split-virus vaccine was less immunogenic than a single dose of whole-virus vaccine. The presence of preexisting antibodies appeared to reduce systemic reactivity. For adequate immunization of a totally unprimed population, a single relatively large and reactive dose of whole-virus vaccine or two, properly spaced, smaller nonreactive doses of either whole-virus vaccine or split-virus vaccine would be required.

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