Hepatitis B (69%), flu (14%), and measles–mumps–rubella (5%) vaccines were considered debatable. Rabies (14%), meningitis (7%), tuberculosis (9%), and Japanese encephalitis (18%) were considered inappropriate. Yellow fever vaccination (19%) was considered an incorrect answer (because there is no particular risk of exposure in Thailand). An expert opinion would have been requested by 22% of PCPs. Appropriate malaria chemoprophylaxis was mefloquine (20%) or atovaquone + proguanil (51%) or doxycycline (21%). Inappropriate protection would have been prescribed by 13%, with 1% prescribing chloroquine

and 12% chloroquine + proguanil. ABT-888 molecular weight Five percent of PCPs chose not to use chemoprophylaxis. An expert opinion would have been requested by 28% of PCPs. The three pieces of priority advice were water hygiene recommendations (81%), hand

hygiene recommendations (65%), and use of condoms (77%). The participating PCPs mostly answered correctly. In contrast with the previous case, only 30% of PCPs would have recommended “repatriation insurance” to this young patient, despite his traveling alone in a country where casualties are frequent. An expert opinion would have been requested by 15% of PCPs. The correct answers for vaccine recommendations were hepatitis A (91%), typhoid (78%), diphtheria–tetanus–poliomyelitis (93%), hepatitis B (92%), yellow fever (51%), and rabies (29%). Tuberculosis (14%) and the measles–mumps–rubella

(19%) vaccines were considered a debatable choice. Meningitis (13%) and flu Baf-A1 (7%) were considered inappropriate answers. The Japanese encephalitis (2%) vaccine and no vaccine recommendation at all (0%) were considered incorrect answers. An expert opinion would have been requested by 25% of PCPs. Appropriate malaria chemoprophylaxis was mefloquine (17%) or atovaquone + proguanil (35%) or doxycycline (11%). Inappropriate protection would have been prescribed by 14% Urease of PCPs, with 9% prescribing chloroquine and 5% prescribing chloroquine + proguanil. Twenty-three percent of PCPs chose not to administer chemoprophylaxis. An expert opinion would have been requested by 24% of PCPs. Scores obtained on the MCQ ranged from 0 to 15 and their distribution is presented in Figure 1. After univariate statistical analysis, 10 variables were associated with a better score for PCPs (Table 4). After multivariate logistic regression, three variables remained associated with a better score: proximity of a vaccination center (p = 0.001), motivation score (p = 0.004), and absence of expert consultation for malaria prophylaxis (p = 0.007) (Table 5). Table 6 presents the statistical link between the MCQ score and the motivation score. The aim of this observational survey was to investigate travel medicine practices in our area and to describe the level of the physicians’ specific knowledge of travel medicine.

Several sensitivity analyses were performed to test the robustness of the findings. First, we changed the lagging windows for the introduction of new drugs from 12–24 months to 6–12 and 24–36 months, respectively. Secondly, we analysed the influence of intervals of >6 months between individual viral load determinations in the data triplets. We used Stata SE 11.0 (StataCorp, College Station, TX) for all analyses. A total of 10 213 participants were seen

in the SHCS from 1 January 2000 to 31 December 2008. Of these, 9802 (96.0%) contributed at least three viral load determinations and constituted the open cohort for the descriptive analyses. The closed cohort is a subgroup restricted to the 5235 participants who had a visit in 2000. The majority of these individuals (91.7%) had entered the cohort prior to 2000. Sixty-four per cent of participants were seen in university out-patient

clinics or large district DNA Damage inhibitor hospitals, Selleckchem PR171 6% in affiliated regional hospitals, and 30% in private practices. Reflecting the changing epidemic in Switzerland, with an increase in the number of HIV-infected immigrants, the open cohort includes more non-Caucasian individuals and fewer persons who have been infected with HIV via injecting drug use (Table 1). The 9802 persons in the open cohort contributed 57 808 years of follow-up. By the end of 2008, 1522 (16%) were lost to follow-up and 903 (9.2%) individuals had died. During follow-up, 197 091 viral load triplets were collected. Participants contributed a median of 38 [interquartile range (IQR) 26–50] viral load determinations and the

median interval between consecutive measurements was 91 (IQR 68–119) days. In 91% of the triplets, the interval was <6 months and in 99% it was <12 months. Thirteen per cent of total follow-up time was prior to starting ART, and 13% was during periods of treatment interruption. Forty-seven per cent of follow-up time was accumulated in the stably suppressed viral load category, 10% in the improving category, 8.5% in the unstable category, 1.9% in the failing category, and 6.8% in the stable failure category. When limited to follow-up times on ART, the corresponding numbers for the viral load categories were 63% stably suppressed, 14% improving, 11% unstable, 2.6% failing, and 9.1% stable failure. Resminostat Figure 1a illustrates trends over time for the viral load categories in the open cohort taking into account the last viral load category per patient and year. The percentage of treatment-naïve individuals remained stable at 13% throughout. This was a result of a balance between the influx of new participants, of whom an increasing proportion were treatment-naïve (2001, 31%; 2008, 44%), and participants starting treatment while followed in the cohort. Treatment interruptions peaked at 15% in 2002 and then declined steadily to 5.4% in 2008.

Double crossover events disrupting C225 pnpA were seen for strains UNE61, UNE64, 1493 and 2483, while a single crossover event disrupted pnpA in strain 819. No tetracycline-resistant colonies were obtained from repeated transformation experiments with pCF5 using strains A198 and C305, confirming previous results that these strains are not naturally competent (Kennan et al., 1998). The phosphorylytic activity of PNPase was measured in the benign and virulent parent strains and in the pnpA mutants (Fig. 2). PNPase activity in the virulent strain A198 was significantly lower than that in the benign strain C305, consistent with the hypothesis

that PNPase acts as a virulence repressor in D. nodosus. The mean this website PNPase activity in the three virulent strains was 25% lower than that in the four benign strains (P<0.05). With the exception of pnpA mutant 2483D3, all of the mutants with the C-terminal deletion in PNPase had significantly reduced PNPase activity compared with the parent strain (Fig. 2). However, this deletion reduced PNPase activity by only 20–50%. This modest reduction in PNPase activity is consistent with similar results from E. coli, where inactivation of the KH and S1 RNA-binding domains also resulted in a modest reduction in PNPase activity (Stickney et al., 2005; Briani et al., 2007).

By contrast, deletion of the S1 domain of PNPase in Salmonella abolished phosphorylytic activity (Clements et al., 2002). The proteases secreted by virulent D. nodosus strains are, in general, more thermostable than the

proteases secreted by benign strains (Depiazzi & Richards, 1979). After heat treatment, the mean remaining protease activity for the four benign strains was significantly lower than that for the three virulent strains (Table 2), as expected. Deletion of the C-terminus of PNPase did not HA-1077 chemical structure alter the thermostability of secreted proteases from the four benign strains, or from the virulent strain UNE61, suggesting that PNPase does not act as a repressor of thermostable protease production. However, the PNPase deletion resulted in a significant reduction in protease thermostability in the virulent strain UNE64. This result is discussed in the next section. The twitching motility of the benign and virulent parent strains and pnpA mutants was measured by determining the colony diameter after growth on TAS agar plates (Fig. 3a and c). The mean colony diameter for the four benign strains, 1.21 cm, was significantly lower than the mean colony diameter for the three virulent strains, 2.66 cm, as expected, since virulent strains have been reported previously to have greater twitching motility (Depiazzi & Richards, 1985).

Cultures of M. capsulatus Bath were grown in NMS (Poret-Peterson et al., 2008), harvested at mid-exponential phase, washed and resuspended to c. 108 cells mL−1 in NMS medium (CH4-only treatment) or NMS medium amended with 0.5 mM sodium nitroprusside (i.e. CH4+SNP treatment)

or 0.25 mM NaNO2 (i.e. CH4+NO2− treatment). Resuspended M. capsulatus Bath cells were exposed to 0.25 mM NaNO2 or 0.5 mM SNP Trametinib supplier for 4 h after which steady-state mRNA levels of norC, norB, cytS, cytL, haoA, rpoB, and nirB were measured by fluorescent real-time PCR (qPCR; iCycler, BioRad). Cells retained activity in the presence of NaNO2 and SNP as measured by rates of CH4 consumption and CO2 production. RNA was extracted using the FastRNA Pro Blue

kit (Qbiogene, Irvine, CA) and converted to cDNA using Superscript III (Invitrogen). Primer sets, qPCR conditions, and product quality assessment were the same as reported previously (Poret-Peterson et al., 2008). N2O production was measured by GC (Shimadzu GC-8A; Hayesep Q column, Alltech) after 24 and 48 h in incubations of harvested and resuspended M. capsulatus Bath cells (at c. 108 cells mL−1) in NMS amended with 0.25 mM NaNO2, 0.5 mM SNP, or 5 mM (NH4)2SO4 in the presence of CH4. To test whether both ammonium and NOx were required to induce N2O production, M. capsulatus Bath was incubated with NaNO2 or SNP plus 5 mM (NH4)2SO4, which induces expression of haoAB and Lumacaftor in vitro cytS genes (Poret-Peterson et al., 2008). In these assays, cells retained >90% viability following centrifugation and resuspension as measured by comparing rates of formate oxidation to CO2 between cells from fresh culture and those resuspended into fresh NMS medium (data not shown). The methanotrophs M. album ATCC 33003, M. sporium ATCC 35069, and Methylocystis sp. Rockwell were previously shown to oxidize NH3 and NH2OH to NO2−, whereas this

activity was not detected in the soil strain, M. methanica Rubra (Nyerges & Stein, 2009). None of these methanotrophs were previously known to harbor genes encoding putative NH2OH oxidoreductases. Analysis by Southern blot revealed that the genomic DNAs from M. album ATCC 33003, M. album BG8, and M. capsulatus Bath produced positive PD184352 (CI-1040) hybridization signals to 32P-labeled fragments of haoA genes, whereas DNAs from the other strains did not (verified by genome sequences; see Table 2). Although Methylocystis sp. Rockwell did not show positive hybridization to haoA gene probes from M. capsulatus Bath or M. album ATCC 33003, examination of its genome sequence revealed haoAB homologues (Tables 1 and 2). No haoAB homologues were found in the genome of M. trichosporium OB3b, suggesting that this bacterium, and likely M. sporium ATCC 35069, converts NH2OH to nitrite through a different pathway (Stein et al., 2010). Analysis of the haoA genes and flanking sequence obtained from M.

This has also been observed in patients treated with nucleos(t)ide therapy (lamivudine, adefovir or tenofovir) with reduced rates of eAg seroconversion in patients with a baseline HBV DNA >7 log10 IU/mL

[102]. During therapy, HBV DNA testing is used to decide whether to continue or stop interferon treatment (see ‘Therapy’, section 4.3 below) [101]. This also applies to nucleos(t)ide therapy where primary nonresponse is defined as a <1 log10 IU/mL drop in HBV DNA level from baseline at 3 months, and response is defined as an undetectable HBV DNA by real-time polymerase chain reaction (PCR) assay within 48 weeks of therapy. Partial virological response is defined as a >1 log10 IU/mL drop in HBV DNA but detectable HBV DNA by real-time PCR assay [101,102]. In HIV-uninfected patients, a partial virological response should lead to a decision about modifying therapy at 24 weeks of therapy for lamivudine and telbivudine (which have selleckchem a low barrier to resistance) and at 48 weeks for entecavir, adefovir and tenofovir (which have a high barrier to resistance) [102]. How this should be applied in coinfected patients is uncertain. Virological breakthrough on treatment, defined as a confirmed increase of >1 log10 IU/mL above nadir HBV DNA level on therapy, means either nonadherence or resistance [102]. The lower limit of detection of the assays used to monitor HBV DNA should be 10–15 IU/mL and this level should also be the aim of treatment

[103]. Measurement of HBV DNA every 6–12 months is sufficient if the patient is not on HBV therapy [104]. 4.2.2.2 Measuring HBV serology during and after therapy. Tacrolimus mouse The ideal outcome of treatment is HBe seroconversion in patients who are HBeAg positive and HBs seroconversion (very rare) in all patients [102]. Once HBV DNA is undetectable, HBeAg and eAb in HBeAg-positive patients and HBsAg in all patients should be tested every 12–24 weeks to pick up seroconversion. It should be noted that there

is no HBV DNA level at which seroconversion from HBeAg positive to negative is completely predictable [105]. Spontaneous or treatment-induced seroconversion from HBsAg positive to negative Acetophenone is associated with ongoing undetectable HBV DNA but, in patients who convert from HBeAg positive to negative, HBV DNA may still be detectable at low levels [102,106]. 4.2.2.3 HBV resistance testing. Resistance testing is becoming more widely available and may be considered as a baseline pretreatment, especially if there is a history of previous exposure to anti-HBV drugs, as a means to inform treatment decisions in those with nonresponse to treatment or with virological breakthrough. A line probe assay for the detection of hepatitis B wild-type virus and a drug-induced mutation using direct sequencing can identify specific resistance mutations [107,108]. Direct sequencing of the HBV polymerase gene can detect variants that are present in 10–20% of the virus population [109].

DNA was released from the bacteria by boiling for 20 min followed by centrifugation Endocrinology antagonist at 10 000 g for 10 min. The supernatant was used

as the DNA template. The LAMP reaction was carried out in a 25-μL reaction mixture with a Loopamp DNA amplification kit (Eiken Chemical Co., Ltd) as described in our previous work (Kubo et al., 2010). The reaction mixture contained 40 pmol (1 μL) each of FIP and BIP, 5 pmol (1 μL) each of F3 and B3 and 20 pmol (1 μL) each of Loop F and Loop B. LAMP reaction was performed at several different temperatures ranging from 55 to 68 °C in 90 min using LA-320C Loopamp real-time turbidimeter (Teramecs, Japan). The best condition for LAMP procedure was at 63 °C and in 60 min. Therefore, all of mixtures were Ion Channel Ligand Library incubated at 63 °C for 90 min, followed by heating at 80 °C for 5 min to inactivate the reaction. Two microlitre of the extracted DNA was used as the template in each reaction mixture. A negative control (a reaction mixture with distilled water instead of DNA template) and a positive control (a confirmed positive sample) were included in each run. Precautions were taken to prevent cross-contaminations. The LAMP product was analysed by three methods including a real-time turbidimeter, agarose gel analysis and naked eye visualization. The LA-320C Loopamp real-time turbidimeter (Teramecs) was used to monitor

the LAMP reaction based on the turbidity of magnesium pyrophosphate at 405 nm, a byproduct of the reaction. The turbidity threshold value for a positive sample was fixed at 0.1, and samples above this threshold value were considered as positive. After amplification, 2 μL of the LAMP product was further separated PJ34 HCl by 2% agarose gel electrophoresis, which was stained with ethidium bromide and visualized under UV light. In addition, 1 μL of SYBR Green I (Invitrogen) was added to the remained LAMP product, a change from orange to fluorescent

green colour was considered as positive. To further distinguish bacterial species, 2 μL of the LAMP product was digested with 10 U of DdeI or HaeIII at 37 °C for 90 min. The digested LAMP product was analysed by 2% agarose gel electrophoresis as described above. A conventional PCR was also carried out with the universal primer set targeting 16S rRNA genes to compare the sensitivity of the LAMP assay. The paired primers were 5′-CCAGCAGCCGCGGTAATACG-3′ and 5′-ATCGG(C/T)TACCTTGTTACGACTTC-3′ (Lu et al., 2000). Twenty-five microlitre of PCR assay contained 2 μL of DNA template, 1 μL of each primer, 2 mM MgCl2, 0.2 mM dNTPs, 2.5 μL of 10 × buffer and 1.25 U Taq HS DNA polymerase (Takara Bio, Shiga, Japan). The reactions were amplified as follows: initial activation of one cycle at temperature 94 °C for 10 min and then followed by 35 cycles at 94 °C for 30 s, 55 °C for 50 s and 72 °C for 2 min. The final extension step was carried out at 72 °C for 10 min. Amplified products were then detected by ethidium bromide staining after 2% agarose gel electrophoresis.

During 2005–2007, a third of women delivered vaginally, half by elective CS and the remainder by emergency CS. In contrast, at the start of the HAART era, two-thirds of women delivered by elective CS. We document geographical variation in mode of delivery in the HAART era, with an increasing proportion of vaginal deliveries, mainly in the United Kingdom, Belgium and the Netherlands. In multivariable analysis of MTCT risk among MCPs with maternal HIV

RNA <400 copies/mL, elective CS was associated with an 80% decreased MTCT risk. However, among women with viral loads <50 copies/mL there were only two transmissions overall. Although clinical trials are the gold standard for clinical care, observational studies often provide initial evidence for trial inception and design. Use of elective CS Selleckchem BKM120 Panobinostat price as a PMTCT intervention is a case in point: the ECS first published results showing an association between reduced MTCT risk and elective CS in 1994 [5],

with subsequent confirmation from a large meta-analysis [9]. Our finding here that the peak elective CS rate occurred in 1999, when the mode of delivery trial was published [8], is probably largely explained by participating clinicians changing their practices before the trial results were released based on the observational evidence they helped to provide; furthermore, some women were concomitantly enrolled in both the trial and the ECS. The somewhat paradoxical finding of a declining elective CS rate in the years immediately following the trial publication may be partly explained by the concurrent implementation of antenatal HAART

instead of mono- or dual therapy for PMTCT, when the first studies suggesting the benefit of HAART for decreasing MTCT risk were published [24–27] and guidelines started to change. In the Netherlands, for instance, the national guideline in 2000 only mentioned an elective CS as a rescue therapy in case of HAART failure or refusal [28]. Other European studies have also documented declining elective CS rates in the HAART era. In an analysis from the French Inositol monophosphatase 1 Perinatal Study involving over 5000 pregnant women receiving antenatal ART and delivering between 1997 and 2004, the elective CS rate declined from 56% in 2000 to 41% in 2004 [4]. In the United Kingdom and Ireland National Study of HIV in Pregnancy and Childhood (NSHPC), the elective CS rate peaked in 1999 at 66%, declining to around 50% in 2006. The emergency CS rate we report here was relatively stable but high and ranged from 15% to 17% in the HAART era; the French Perinatal Study also reported stable emergency CS rates between 1997 and 2004, but higher at around 29% [4].

The different frequencies of HLA-B*5701 found in patients from different African countries strongly suggest greater utility of HLA-B*5701 screening in some African groups compared with others. Although ethnic-based

pharmacogenetic screening in UK clinics with diverse populations is unlikely to be practical and also likely to be ethically unacceptable, our figures add to the need for caution when considering screening in diverse African settings. Despite an overall sample size of 1502, only two sub-divisions had a sufficiently large sample to allow meaningful interpretation of the prevalence rate [White/Eurasian and Niger-Congo with prevalence rates of 7.95% (CI 5.88%–10.02%) and 0.52% (CI 0.18%–1.52%), respectively]. On the basis of previous GDC 0199 work, we sub-divided our African patients according to linguistic index that language groups might reflect genetic structure [9]. However, more recent data suggest that this

may not necessarily be true in all settings and particularly not African ones [14]. In contrast, a recent, well-publicized study of 121 African populations demonstrated genetic clustering across the Niger-Congo R428 (Niger-Kordofanian) linguistic populations [15]. Our data, where both Ugandan and Zimbabwean populations were classified as Niger-Congo (Bantu) but had very different HLA-B*5701 prevalences, demonstrate the difficulties in using such classifications to distinguish populations either in genetic studies of specific, non-neutral alleles. Our study was not able to distinguish northern (Nilotic) Ugandans from Bantu Ugandans, so it is possible that the different rates among

Zimbabweans and Ugandans were because of cross-classification. However, a significant majority of Ugandans in the United Kingdom are thought to be Bantu and HLA-B*5701 frequency among Nilotics has been reported to be lower than among Bantu [4]. The 244 unclassifiable subjects underline the difficulties in basing decisions on these self-reported measures of ethnicity. Only one of the three HLA-B*5701 positive subjects in the Niger-Congo sub-division self-reported as genetically homogenous reflecting the potential of genetic admixture to complicate analysis. Future studies may consider the use of ancestry information bio-markers to define population groups more accurately. The single false-positive result in a local laboratory reinforces the need for robust laboratory quality assurance. It is reassuring that Sequence specific primer (SSP) methodology failed safe by identifying the patient as HLA-B*5701 positive; by doing so it ensured patient safety was maintained. In the present study, HLA-B*5701 prevalence in the UK was similar to previously reported rates in White HIV-infected subjects but considerably lower than those reported in Black HIV-infected subjects, probably as a result of the large proportion of Black subjects that were of African origin. In addition, 99.

, 2002; Nakasone et al., 2007), which is the most abundantly secreted protein in both pathogens. The RPLA test is more sensitive (detection limit: 1 ng mL−1) than the IC test (detection limit: 4 ng mL−1), but requires overnight incubation. Although Dulbecco’s modified Eagle’s medium (DMEM) is commonly used to detect EspB from EPEC or STEC, we noticed

that some strains grew poorly and sometimes did not grow at all in the medium, even though they were shown to possess the eae gene by PCR. Therefore, using DMEM may Apoptosis Compound Library purchase produce false-negative results due to small amounts of or no EspB being produced. To resolve this problem, a medium in which bacteria can grow and produce EspB is required. If a growth medium that enhances both bacterial growth and EspB production could be created, the sensitivity of the RPLA and/or the IC test for detecting EPEC and/or STEC might be increased. Although various media and/or culture conditions have been considered for the enhancement of the

proteins secreted by EPEC and STEC (Haigh et al., 1995; Kenny et al., 1997; Beltrametti et al., 1999; Yoh et al., 2003), a medium that works equally well for both pathogens has been identified. Considering the environmental conditions found in the human body, bacterial growth and the secretion of Esp proteins might be affected by bile acid or detergents. In this report, we considered a medium supplemented with various detergents and examined its selleck chemicals llc effects on EspB production. Our results suggested that the detergent-supplemented medium enhanced EspB production in the EPEC and STEC strains and that this new medium is a convenient tool for promoting the expression of EspB. E2348/69 (O127:H6) and EDL933 (O157:H7) were used as standard EPEC and STEC strains, respectively. The other strains used in this study were isolated

from patients with diarrhea in a variety of countries, as described previously (Lu et al., 2002). The strain of each isolate was determined using a standard biochemical test O-methylated flavonoid and the PCR method described by Toma et al. (2003). The characteristics of the organisms used in this study are listed in Table 1. To elucidate the optimal concentrations of the detergents for EspB detection, each detergent was serially diluted from 1.5% (w/v) with Luria–Bertani (LB) broth and incubated with the reference strains at 37 °C for 15 h. After incubation, the OD at 600 nm was adjusted to 0.7 (c. 1 × 108 CFU mL−1) with LB broth. The culture was then centrifuged at 5000 g for 15 min, and the supernatant proteins were precipitated by the addition of trichloroacetic acid at 10%, as described by Yoh et al. (2003). The resultant pellet was resuspended in 50 μL of 1 M Tris-HCl buffer (pH 7.6), and EspB was detected using Western blotting, the RPLA test, or the enzyme-linked immunosorbent assay (ELISA). The RPLA test was carried out as described elsewhere (Lu et al., 2002).

However, the rates

of efavirenz teratogenicity reported by the US-based Antiretroviral Pregnancy Registry are consistent with those reported internationally. For example, a recent BIBW2992 publication by Bera et al. [49] reports experience with 818 HIV-infected pregnant women at a regional South African hospital exposed to efavirenz during pregnancy. In the 807 live births, they found a teratogenicity rate of 3.3% (95% CI 1.2–7.0%) for first trimester exposures to efavirenz and 2.6% (95% CI 1.5–4.2%) for second and third trimester exposures. These rates are similar to the baseline rate used in this analysis (2.72%). In our analysis, the estimated range of the rate of teratogenic events with efavirenz used in sensitivity analysis (1.6–4.9%) extends above and below the US background rate of 2.72%. Thus, estimates of excess teratogenic events compared with the background number of events includes both negative and positive values (range −72.98 to 142.05 events per 100 000 women), depending on the rates of pregnancy and the teratogenicity of efavirenz. This suggests that use of efavirenz may have less of an impact on teratogenicity compared with background rates than this analysis predicts. More data are needed

to better estimate the true risk of teratogenic events in pregnant women receiving efavirenz as well as other antiretroviral medications. The benefits and risks – both known and unknown – of ART should be discussed with Epigenetics inhibitor HIV-infected women of childbearing age [48]. These discussions should address not only the potential survival advantage for the infected woman and the potential for reduction of mother-to-child transmission, but also the possible risks with respect to toxicity, pregnancy outcomes, and the health of the fetus or infant. Clinical Tryptophan synthase decisions about using efavirenz-based treatment present a potential trade-off between life expectancy gains in women

and risk of teratogenicity; these results should inform discussions between women and their health care providers. This research was supported in part by the National Institute of Allergy and Infectious Diseases (grants K24AI062476 and R37AI42006). Data in this manuscript were collected by the Women’s Interagency HIV Study at the following centres: New York City/Bronx Consortium (Kathryn Anastos); Brooklyn, NY (Howard Minkoff); Washington DC Metropolitan Consortium (Mary Young); The Connie Wofsy Study Consortium of Northern California (Ruth Greenblatt); Los Angeles County/Southern California Consortium (Alexandra Levine); Chicago Consortium (Mardge Cohen); Data Analysis Center (Stephen Gange).