These data show declines in HSV-2 seroprevalence, suggesting that the trajectory of increasing HSV-2 seroprevalence in the United States has been reversed. Seroprevalence of HSV-1 decreased but the incidence of genital herpes caused by HSV-1 may be increasing.

No abstract

A necessary role for cytotoxic T lymphocytes in protection againstMycobacterium tuberculosis (MTB) has been suggested by studies of the ␤2-microglobulin-deficient mouse, which is unable to present antigens through MHC class I and class I-like molecules and invariably succumbs early after infection. To identify the relative contributions of distinct putative MHC class I-dependent cell populations in protection against tuberculosis, we compared a variety of gene-disrupted mouse strains for susceptibility to MTB infection. Among the strains tested, the most susceptible mice, as measured by survival time and bacterial loads, were the ␤2-microglobulin ؊͞؊ , followed by transporter associated with antigen processing deficient (TAP1 ؊͞؊ ), CD8␣ ؊͞؊ , perforin ؊͞؊ , and CD1d ؊͞؊ mice. These findings indicated that (i) CD8 ؉ T cells contribute to protection against MTB, and their protective activity is only partially dependent on perforin; (ii) ␤2-microglobulin-dependent T cell populations distinct from CD8 ؉ T cells also contribute to anti-MTB immunity; and (iii) protective immune mechanisms are predominantly TAP-dependent, although TAP-independent mechanisms also contribute to protection. Because CD1d-deficient animals were fully resistant to MTB, other TAP-independent mechanisms must contribute to protection. We suggest here that both classical and nonclassical MHC class I-restricted T cells, distinct from CD1d-restricted cells, may be involved in protective immune responses against tuberculosis.CD8 ϩ T cells ͉ perforin ͉ ␤2-microglobulin ͉ transporter associated with antigen processing ͉ CD1d