Human papillomavirus type 16 (HPV-16) genotype variants have been the subject of several investigations, but study participants have rarely been sampled more than once. In this study, among a cohort ...of human immunodeficiency virus (HIV)-infected adults, HPV-16 variants were investigated in samples collected concurrently from the anus and cervix, as well as in serial samples collected from the same anatomical site at 12-month intervals. HPV-16 variants in stored extracts of cervical and anal samples were determined from subjects with multiple visits and at least one sample positive for HPV-16. Seven polymorphic nucleotide positions within the E6 region were analysed by pyrosequencing to determine genotype variants. Of 364 samples examined, 176 anal and 39 cervical swabs from 84 different subjects yielded unequivocal sequences of eight major HPV-16 variants. Eight samples contained probable novel HPV-16 variants and in one sample two variants were detected. In eight out of 29 (27.6%) anal-cervical sample pairs positive for HPV-16, discordant variants were found. From 57 anal and nine cervical sample series of HPV-16-positive samples, a change in HPV-16 variant status over time was seen in nine (13.6%) instances (seven anal and two cervical) from eight different participants. Changes in HPV-16 variants in HIV-infected adults were seen most frequently when different anatomical sites were sampled, but were also observed over time.
To characterize health care workers with the acquired immunodeficiency syndrome (AIDS) in the United States and to evaluate the role of occupational transmission of the human immunodeficiency virus ...(HIV).
National AIDS surveillance data.
Health care workers with AIDS are reported to the Centers for Disease Control by state and local health departments. Health care workers who do not report a nonoccupational risk for HIV infection are termed undetermined risk cases and are investigated by health departments using a standard protocol.
Through June 30, 1990, there were 5425 cases of AIDS in health care workers reported in the United States. Three of these workers developed AIDS following well-documented occupational exposure to HIV-infected blood. Of the 539 health care workers initially reported without a nonoccupational risk, follow-up investigations were completed for 303. Nonoccupational risk factors were established for 237 (78.2%) of the 303 investigated health care workers; 66 workers (21.8%) remained in the undetermined category. Follow-up information was incomplete for 236 health care workers who also remained in the undetermined category, resulting in 5120 health care workers (94.4%) with AIDS with nonoccupational risks for HIV infection. Overall, health care workers were more likely than non-health care workers with AIDS to have an undetermined risk for HIV infection (5.6% vs 2.8%; P less than .001). While many of the 66 investigated health care workers had jobs involving contact with patients and/or potential contact with blood, none reported percutaneous, mucous membrane, or cutaneous exposures to blood or body fluids known to be infected with HIV.
Surveillance data suggest that most health care workers with AIDS acquired their HIV infection through a nonoccupational route.
To clarify the effect of cigarette smoking on the development of conditions associated with HIV infection.
Prospective and retrospective cohort study, with interview and examination twice a year ...since 1988.
Data on 516 HIV-infected men from cohorts of homosexual and bisexual men in San Francisco, Denver and Chicago, who were repeatedly interviewed and examined between 1988 and 1992, were analysed. After excluding men who did not have well-defined dates of seroconversion and those who were classified as ex- or intermittent smokers, 232 men remained for analysis: 106 were smokers and 126 were non-smokers. Univariate and Kaplan-Meier survival analyses were performed to assess the relationship between cigarette smoking and loss of CD4+ T-lymphocytes, diagnosis of any AIDS-defining illness, and specific diagnosis of Kaposi's sarcoma, Pneumocystis carinii pneumonia (PCP), oral candidiasis, hairy leukoplakia, and community-acquired pneumonia.
By univariate analyses, cigarette smoking was not associated with clinical AIDS, loss of CD4+ cells, Kaposi's sarcoma or PCP, but was significantly associated with oral candidiasis relative risk (RR), 1.32; 95% confidence interval (CI), 1.02-1.70, hairy leukoplakia (RR, 1.51; 95% CI, 1.15-1.99), and community-acquired pneumonia (RR, 2.62; 95% CI, 1.30-5.27). Dose-response effect was also evident for these three conditions (all P < 0.01). Kaplan-Meier survival analysis indicated no association between cigarette smoking and time of progression to clinical AIDS, Kaposi's sarcoma (KS), or PCP (P = 0.62, 0.54 and 0.11, respectively) but showed that cigarette smokers developed oral candidiasis, hairy leukoplakia, and pneumonia more quickly than non-smokers (P = 0.031, 0.006 and 0.009, respectively).
Cigarette smoking was not associated with an increased likelihood or rate of developing KS, PCP or AIDS, but was associated with developing community-acquired pneumonia, oral candidiasis, and hairy leukoplakia in these HIV-infected men.
To determine the use of AIDS drugs and therapies by populations with relatively good access to health care.
Prospective cohort study, with interview and examination twice a year since 1988.
Two ...public-health departments (San Francisco Department of Health and Denver Disease Control Service) and a private clinic (Howard Brown Memorial Clinic, Chicago).
HIV-seropositive homosexual and bisexual men in San Francisco (311 men), Denver (120 men) and Chicago (59 men).
HIV counseling and testing at each visit.
Time and duration of use of drugs used for AIDS and Pneumocystis carinii pneumonia (PCP) treatment and prophylaxis.
Zidovudine and pentamidine use increased from 1987 through 1989 in all three cities. In San Francisco in 1987, only 17 out of 110 (15%) HIV-seropositive men without AIDS reported taking zidovudine. By 1990, over 90% of AIDS patients and approximately 80% of HIV-seropositive men with low CD4+ cell counts (< 200 x 10(6)/l) had taken zidovudine; most men who by 1990 had never taken zidovudine (82%) or PCP prophylaxis (95%) had not been recommended these therapies because they did not have symptoms and their absolute CD4+ cell counts were > 200 x 10(6)/l. However, overall in the three cities, only 68% of the AIDS patients and 63% of the men with low CD4+ cell counts had taken zidovudine for more than 6 months by 1990. Most men who had stopped taking zidovudine (67%) did so because of toxicity; however, 64% of respondents gave reasons other than drug toxicity as a or the sole reason why they discontinued zidovudine.
AIDS therapeutic and prophylactic drugs were increasingly (and appropriately) recommended to and accepted by these cohorts after 1987, but had limited consistent use because of toxicity, adverse side-effects, and several other less readily appreciated reasons. These data do not indicate that zidovudine use in San Francisco would mainly account for the observed slowing in the rate of increase of AIDS cases in homosexual and bisexual men in this city after 1987.
To assess a hypothesized trend that persons recently infected with the human immunodeficiency virus (HIV) may have more rapid declines in absolute CD4 T-lymphocyte (CD4+ cell) counts than those who ...were HIV-infected in earlier years, sequential CD4+ cell counts in three groups who had definable dates of HIV seroconversion between 1978 and 1992 were reviewed. The CD4+ cell counts examined were from some of the longest extant studies in the United States: 100 homosexual and bisexual men engaged in ongoing observational cohort studies in San Francisco, Denver, and Chicago since 1978 (Group 1); 89 persons in South Carolina infected after 1986 (Group 2); and 155 injecting drug users participating in an observational cohort study in Baltimore since 1988 (Group 3). For all groups, individually and in the aggregate, mean CD4+ cell counts declined rapidly in the first year after HIV infection and then stabilized. However, there was no clear trend for lower (or higher) CD4+ cell counts by fixed time after HIV seroconversion among those seroconverting in recent compared with earlier calendar years. These data do not support a hypothesized trend for more rapid loss of CD4 T lymphocytes--and, by implication, more pathogenic strains of HIV-1--among persons acquiring HIV infection in recent years.
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