Prevalence of transmitted drug resistance associated mutations and HIV-1 subtypes in new HIV-1 diagnoses, U.S.-2006.

OBJECTIVE: To determine the distribution of HIV-1 subtypes and the prevalence of transmitted drug resistance-associated mutations (TDRM) among persons newly diagnosed with HIV-1 infection in the United States. METHODS: We used sequence data from Variant, Atypical, and Resistant HIV Surveillance (VARHS) collected from newly diagnosed persons in 10 states and 1 county health department in 2006. To evaluate TDRM, we used a mutation list for surveillance of TDRM appropriate for the primarily subtype B HIV epidemic in the United States. RESULTS: Sequences were obtained from 2030 of 10,860 persons newly diagnosed with HIV in 11 surveillance areas. Mutations associated with transmitted drug resistance occurred in 292 (14.6%) persons; TDRM associated with a specific drug class occurred in 156 (7.8%) for non-nucleoside reverse transcriptase inhibitors, 111 (5.6%) for nucleoside reverse transcriptase inhibitors and 90 (4.5%) for protease inhibitors. There were no significant differences in prevalence of TDRM by demographic characteristic. The HIV-1 subtype B was the most prevalent subtype occurring in 1922 (96.2%) persons; subtype C (1.3%) was the most prevalent non-B subtype. CONCLUSION: We presented a clade B-optimized mutation list for evaluating surveillance of TDRM in the United States and analyzed the largest collection of sequence data obtained from individuals newly diagnosed with HIV. The prevalence of TDRM in persons newly diagnosed with HIV is higher than in previous U.S. studies; however, this is not necessarily a significant trend. Continued reporting of sequence data for public health purposes from all sources will improve representativeness and accuracy in analyzing trends in transmitted drug resistance and genetic diversity.

HIV testing frequency among men who have sex with men attending sexually transmitted disease clinics: implications for HIV prevention and surveillance.

OBJECTIVES: To describe trends in the occurrence and frequency of HIV testing among men who have sex with men (MSM) receiving care in 4 US sexually transmitted disease (STD) clinics and to define factors associated with HIV testing frequency and positivity. STUDY DESIGN: Routine clinical encounters during 57,131 visits by MSM to STD clinics in 4 cities (Seattle-King County, San Francisco, Denver, and District of columbia), 2002-2006, were examined. RESULTS: From 2002 to 2006, a city-specific median of 69.1% of presumptive HIV-uninfected MSM were tested for HIV, of which, a median of 86.7% had previously tested (4.5% unknown) and a median of 3.9% were newly diagnosed with HIV. Between 2002 and 2006, the median percentage of tested MSM who reported no previous HIV testing decreased from 9.4% to 5.4% (P = 0.01) and the city-specific median intertest interval decreased from 302 to 243 days (P = 0.03). Among MSM with newly diagnosed HIV, the median intertest interval decreased from 531 days in 2002 to 287 days in 2006 (P = 0.001). Predictors of newly diagnosed HIV infection included the following: younger age, longer intertest interval, black or Hispanic race/ethnicity, clinic in San Francisco, and concurrent diagnosis with a bacterial STD. CONCLUSIONS: In MSM seen at 4 STD clinics, the percentage of never previously HIV tested is decreasing and MSM are testing more frequently.

Cytochrome oxidase inhibition induced by acute hydrogen sulfide inhalation: correlation with tissue sulfide concentrations in the rat brain, liver, lung, and nasal epithelium.

Hydrogen sulfide (H2S) is an important brain, lung, and nose toxicant. Inhibition of cytochrome oxidase is the primary biochemical effect associated with lethal H2S exposure. The objective of this study was to evaluate the relationship between the concentration of sulfide and cytochrome oxidase activity in target tissues following acute exposure to sublethal concentrations of inhaled H2S. Hindbrain, lung, liver, and nasal (olfactory and respiratory epithelial) cytochrome oxidase activity and sulfide concentrations were determined in adult male CD rats immediately after a 3-h exposure to H2S (10, 30, 80, 200, and 400 ppm). We also determined lung sulfide and sulfide metabolite concentrations at 0, 1.5, 3, 3.25, 3.5, 4, 5, and 7 h after the start of a 3-h H2S exposure to 400 ppm. Lung sulfide concentrations increased during H2S exposure and rapidly returned to endogenous levels within 15 min after the cessation of the 400-ppm exposure. Lung sulfide metabolite concentrations were transiently increased immediately after the end of the 3-h H2S exposure. Decreased cytochrome oxidase activity was observed in the olfactory epithelium following exposure to > or = 30 ppm H2S. Increased olfactory epithelial sulfide concentrations were observed following exposure to 400 ppm H2S. Hindbrain and nasal respiratory epithelial sulfide concentrations were unaffected by acute H2S exposure. Nasal respiratory epithelial cytochrome oxidase activity was reduced following acute exposure to > or = 30 ppm H2S. Liver sulfide concentrations were increased following exposure to > or = 200 ppm H2S and cytochrome oxidase activity was increased following inhalation exposure to > or = 10 ppm H2S. Our results suggest that cytochrome oxidase inhibition is a sensitive biomarker of H2S exposure in target tissues, and sulfide concentrations are unlikely to increase postexposure in the brain, lung, or nose following a single 3-h exposure to < or = 30 ppm H2S.