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Background: Previous population-based estimates in the United States have shown a relatively high prevalence of hepatitis E virus (HEV) antibody. We sought to determine whether changes in the prevalence of HEV antibody have occurred over time., Methods: We analyzed data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) and NHANES III (1988-1994). Using the same serologic assay, we compared the estimated anti-HEV immunoglobulin G (IgG) prevalence and risk factors for antibody positivity for the 2 periods., Results: The prevalence of HEV antibody among those aged ≥6 years declined from 10.2% (95% confidence interval [CI], 9.1%-11.4%) during 1988-1994 to 6.0% (5.2%-6.8%) during 2009-2010, and the prevalence for those of US birth ranged from 9.6% (8.4%-10.9%) to 5.2% (4.4%-6.2%). Among US-born persons, the estimated HEV antibody prevalence declined significantly for all subgroups of age, sex, region of residence, and number of persons per room in the household; significant declines also were observed for persons at or above poverty level and for persons of non-Hispanic white, non-Hispanic black, and Mexican American race/ethnicity. No clear associations with food consumption were found., Conclusions: The anti-HEV prevalence is declining in the United States. Although the decline suggests a decrease in exposure to HEV over time, the risks associated with exposure remain unknown., (Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.)

Host human leukocyte antigens (HLAs) integrated into the human immunodeficiency virus (HIV) type 1 envelope could theoretically determine, as in tissue transplants, whether HIV-1 is "rejected" by exposed susceptible persons, preventing transmission. HLA discordance (mismatch) was examined among 45 heterosexual partner pairs in which at least 1 partner was HIV-1 infected and exposure or transmission between partners had occurred. Immunologic discordance at class II HLA-DRB3 (present in the HIV donor partner but absent in the recipient partner) was associated with lack of transmission of HIV-1. Eight (35%) of 23 partner pairs in which HIV-1 transmission did not occur were immunologically discordant at HLA-DRB3, compared with 0 of 11 partner pairs in which HIV-1 transmission did occur (P=.027). Further investigation of the roles of class II HLAs in HIV-1 transmission and as possible components of HIV-1 vaccines should be pursued.

In the United States, human immunodeficiency virus (HIV) type 1, group M, subtype B is the predominant subtype. A cross-sectional study of HIV-infected patients at the Bronx-Lebanon Hospital Center, Bronx, NY, between September 1997 and February 1998 identified 3 (1. 2%) of 252 persons infected with non-B subtypes: subtypes A and F, 1 each, and 1 potential recombinant subtype B(env)/F(prt). All 3 persons were born in the United States and tested positive for HIV antibodies between 1988 and 1997 while living in the Bronx. None reported travel to other countries, receipt of blood products, or drug injection. This study is among the first to indicate probable transmission of non-B HIV-1 subtypes in the United States. The occurrence of non-B HIV-1 subtypes in long-term US residents without a history of foreign travel may have implications for the evaluation and development of antiretroviral drugs, vaccines, and tests intended for use in the United States to diagnose HIV infection and screen blood.

The reasons for recent declines in AIDS incidence and mortality may include advances in treatment, but these may be confounded by earlier declines in the incidence of human immunodeficiency virus (HIV) infection. To determine whether the declines in AIDS and mortality may, in part, stem from wider use of combination antiretroviral therapy, 622 HIV-positive men with well-characterized dates of seroconversion were followed. In this group, combination therapy came into widespread use in only 1996. In a Cox proportional hazards model, the 1996 calendar period was significantly associated with slower progression to AIDS (relative hazard [RH]=0. 19, 95% confidence interval [CI], 0.05-0.69, P=.01) and death (RH=0. 45, 95% CI, 0.21-0.95, P=.04). Declines in incidence of HIV infection, changes in HIV virulence, and end-point underreporting cannot fully explain the decline in AIDS and death in 1996. The introduction of combination antiretroviral therapy as the standard of care may already have had measurable effects.

Temporal changes in the lifetime occurrence of opportunistic infections and malignancies among 1115 homosexual men diagnosed with AIDS were examined. Information from the AIDS surveillance registry, hospital pathology and microbiology logs, patient chart reviews, cancer registries, and death certificates was used to calculate the frequency of specific opportunistic infections and malignancies as lifetime (initial or subsequent) diagnoses. The most common lifetime diagnoses were Pneumocystis carinii pneumonia (PCP; 66.5%), Kaposi's sarcoma (KS; 50.7%), disseminated Mycobacterium avium complex (DMAC) infection (29.6%), and cytomegalovirus (CMV) infection (19.6%). From 1981 to 1990, there was a significant decrease in the rate of KS (P = .003) and a significant increase in the rate of DMAC infection (P = .03). PCP decreased during 1985-1990 (P = .009), while CMV infection increased from 1987 through 1990 (P = .03). Thus, KS and PCP have declined over time, while DMAC and CMV are causing substantial and increasing morbidity among AIDS patients.

The interaction of herpes zoster and the human immunodeficiency virus (HIV) was evaluated in a cohort study of 287 homosexual men with well-defined dates of HIV seroconversion and 499 HIV-seronegative homosexual men. The incidence of herpes zoster was significantly higher among HIV-seropositive men (29.4 cases/1000 person-years) than among HIV-seronegative men (2.0 cases/1000 person-years); the overall age-adjusted relative risk (RR) was 16.9 (95% confidence interval [CI], 8.7-32.6). When compared with that of age-matched population controls from 1945 to 1959, the incidence of zoster was significantly higher among seropositive men (RR, 26.7; 95% CI, 19.3-37.1) and slightly higher among seronegative men (RR, 1.85; 95% CI, 1.0-3.3); the latter may reflect increasing background rates over several decades. The risk of herpes zoster was not associated with duration of HIV infection and was not predictive of faster progression to AIDS.

From a prospective cohort study, 24 asymptomatic men were identified who had been antibody positive for human immunodeficiency virus (HIV) for at least 5 years (median = 9.1) with CD4+ lymphocyte counts greater than or equal to 400 cells/mm3. Of these "nonprogressors", 23 (96%) had evidence of HIV infection by either HIV culture or the polymerase chain reaction (PCR) for HIV DNA, although only 1 (4%) had a positive assay for HIV RNA (by PCR) and no one was positive for p24 antigen. Compared with 24 antibody-negative men and 14 men with AIDS, nonprogressors had higher CD8+ counts and lower natural killer cell activity. Nonprogressors had higher beta 2-microglobulin levels than did seronegative controls, suggesting some degree of immune system activation. Compared with men with AIDS, nonprogressors seemed to have a stronger antibody response to six different HIV-related proteins but did not differ significantly in neutralizing antibody or antibody-dependent cellular cytotoxic activity.

To evaluate the correlation of detection of human immunodeficiency virus (HIV) by polymerase chain reaction (PCR) with detection of HIV antibody, 271 simultaneous serum and peripheral blood mononuclear cell samples were examined from 242 persons whose activities placed them at increased risk for HIV infection: 142 from homosexual men, 86 from hemophilic men, and 43 from heterosexual partners of HIV-infected persons. PCR was performed using the gag region primer pair SK38/39 and the env region primer pairs SK68/69 and CO71/72. Amplified HIV DNA was detected using specific oligomer probes. Of 63 HIV antibody-positive samples, 58 (92%) had HIV DNA by PCR. Of 208 HIV antibody-negative samples, 7 (3.4%) had HIV DNA by PCR. On follow-up, 4 of the latter persons were seropositive when next tested; 2 were well and antibody- and PCR-negative; 1 had died of a stroke before retesting. Thus, PCR detects HIV in most antibody-positive persons; detection is increased by use of multiple primer pairs. PCR-positive antibody-negative specimens may indicate HIV infection in which antibody has not yet developed or may be false-positive PCR results. When PCR is discordant with HIV antibody, testing of additional specimens and clinical follow-up are necessary to assess HIV infection status.

The probability that any single episode of genital-genital or anogenital sexual intercourse will result in transmission of HIV may be determined by multiple biologic factors of the infectious person, the virus itself, and the exposed susceptible person. Some of these factors are known or suspected (figure 1), and they may explain observed differences in the sexual transmission of HIV in different parts of the world, notably in Africa, where genital ulcerative disease is probably influencing the epidemiology of HIV. Several studies have shown that infection in partners of HIV-infected persons is not determined solely by numbers of sexual encounters; on the contrary, HIV-infected partners have usually had fewer sexual encounters with infectious mates than have noninfected partners. Thus, sexually active persons should be cautioned that, to our knowledge, there are no nonsusceptible persons and that any single unprotected sexual encounter may lead to HIV transmission. Research into biologic factors that modulate HIV transmission continues to be hampered by difficulties in identifying HIV transmitters and nontransmitters, infective and noninfective variants of HIV (if the latter exist in vivo), and persons relatively more or less susceptible to HIV infection. However, as the number of partner studies and the number of those enrolled in them increase, a progressively clearer idea of the biologic determinants of sexual transmission of HIV should emerge.