Prevalence and incidence data are important information in the design and evaluation of programs and interventions for sexually transmitted infections (STIs) and in interpreting changes in HIV epidemiology. The World Health Organization (WHO) periodically generates estimates to assess the global burden of four of the most common curable sexually transmitted infections.1 Strategies for preventing and controlling HIV infection based on behavioral risk factors can be improved by aggregating information about biological determinants that contribute to HIV transmission. From a policy perspective, treatment of curable STIs is an essential part of primary health care and should continue to be promoted as one component of HIV control programs in communities in which the burden of STIs is substantial.2 In addition, bacterial vaginosis is associated with increased risk of multiple adverse outcomes, including transmission and acquisition of human immunodeficiency virus type 1 (HIV-1) and STIs.3 Furthermore, HIV-infected persons may have a modified clinical course of STIs owing to decreased immunity, leading to poor quality of life and increased morbidity and mortality.4

The development of highly active antiretroviral therapy (HAART) has led to a reduction in mortality and morbidity rates among people living with HIV (PLHIV).1,2 Early initiation of HAART will lead to near-normal quality of life and lifespan5 and reduce plasma viral load, which is a primary determinant of the risk of transmission.5,6 Moreover, reduction of transmission to sexual partners among those initiating HAART will depend upon viral load in plasma and genital tract.1,7 Although rare, even with the infected partner on effective HAART and undetectable viral load, HIV may still be transmission has been documented.7,8 Thus, the risk is substantially reduced, but it is not completely eliminated. Rapid development in the field of HAART has led to a reduction in morbidity and mortality among PLHIV. There is a growing concern over sexual risk behavior (multiple partners or unprotected sex) of PLHIV on HAART. Changes in sexual risk behavior of PLHIV after initiation of HAART might have important implications on the way counseling may be designed and implemented. Increased sexual risk behavior with therapy will be a matter of great concern from the perspective of preventing transmission. If not intervened, it may further fuel the epidemic.9 Optimism related to the success of HAART in slowing disease progression, reducing viral load, and improving health status (significant improvements occurred across general health perception; physical, social, and cognitive functioning; pain; mental health; energy; and fatigue) might be crucial factors determining sexual risk behaviors.10,16

Being HIV-infected is hypothesized to be a sufficiently dramatic experience to destroy any unfounded belief in the effectiveness of the strategy of protection.¹¹

The study on the prevalence of STIs in WLHIV is of great importance as it provides information on epidemiological and social profile, in addition to sexual risk behavior. It also generates data that can be used in the implementation of prevention and treatment programs.8,12 Delay to detect precancerous lesions may have harmful consequences, mainly in HIV-infected women due to faster disease progression.¹³ Although early diagnosis of precancerous lesions can be achieved by the relatively simple Papanicolaou test, cancer is often diagnosed late.14 Additionally, Davidson et al. have reported that a significant proportion of women with invasive carcinoma had a negative cytology history before the onset of disease.15

This study aimed to determine the prevalence rates of STIs such as Chlamydia trachomatis, Neisseria gonorrhoeae, syphilis, hepatitis B and C, and high-risk HPV (HR-HPV) in WLHIV who attended a reference center for STI/AIDS in Brazil.

One hundred fifty-one women receiving HIV care at the reference center for STI/AIDS were enrolled in the study between February 2014 and October 2015. Sociodemographic characteristics and risk-taking behaviors of the participants are presented in Table 1. The median age at enrollment was 41 years (SD = 10.8). Among the participants, 35.7% had been infected with HIV for 10–20 years, 5% had a CD4 count less than 200 cells/mm3, 61.6% had an undetectable HIV viral load, and 81.1% were currently on HAART; 15.4 % of women reported 21 or more lifetime sexual partners, and 22.7% reported onset of sexual activity at the age of 15 years or younger, 68% reported a history of receptive anal intercourse, 49% reported use of condoms during all sexual intercourse, and 19.3% were active cigarette smokers. In comparison, 35.6% and 24.7% had a history of alcohol ingestion or drug use, respectively (Tables 2 and 3).

A total of 59.2% had at least one diagnosed STI at the time of the first clinic visit, with the most common being condyloma acuminatum, 31.0% had clinical forms of anogenital HPV, 10.0% had syphilis, 5.0% had trichomoniasis, 3% were infected by Chlamydia trachomatis, 8% by Neisseria gonorrhoeae, 1.0% had hepatitis B, and 1.0% hepatitis C. Fig. 1 shows the prevalence of STIs at the time of the first clinic visit.

Fig. 1.

Prevalence of STIs at the time of the first clinic visit.

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Cervical cytological abnormalities (defined as ASC-US or higher degree of abnormality) were found in 6.7% of women, 28 (18.5%) underwent cervical biopsy and had cervical intraepithelial neoplasia (CIN), some of whom had normal cytology. Out of 28 biopsies performed, 18 (11.9%) revealed high-grade squamous intraepithelial lesion (HSIL), and 10 (6.6%) low-grade squamous intraepithelial lesion (LSIL). Overall, HR-HPV (HPV 16, 51, 52, 53, 45, 18, 39, 59, 58, 33, 31, 68 and 35) types were present in 73 (48.3%) patients.

Globally, the burden of HPV infection, causing cervical neoplasia, is high in developing countries. The oncogenic nature of the genotypes differs in each region of the world. A Brazilian study published in 2013 identified that 170 of 172 (99%) women with cancer were found to be positive for HPV.28 The most frequent HPV genotypes observed were HPV16 (77.6%), HPV18 (12.3%), HPV35 (5.9%), HPV31 (8.8%), and HPV33 (7.1%), most often (75%) in isolation.29 The most frequent HR-HPV In our study 16 (13.5%), 51 (9.5%), 52 and 53 (both 5.6%) were the prevailing genotypes.

Overall, studies showed that the prevalence of HPV infection in WLHIV in Brazil is high, whereas that of CIN is low. These findings may be due to the vast majority of studies being conducted in regions that are more developed, where HIV-infected women have better follow-up and use HAART more correctly, thus with less risk to development cervical lesions.30 WLHIV were 4.5 times more likely than uninfected women to develop cervical intraepithelial neoplasia.24,25 The rate of high-risk HPV in our study was quite high, 48.3% (73/151). This rate was even higher in women who had sexual intercourse for the first time before age 15 (69.7%) and in those who had more than 50 partners throughout their life (58.6%). A cohort study in Denmark found an HPV rate of 28% among HIV-infected women.26

The prevalence of CIN lesions (18.5%) among WLHIV in this study was very similar to that reported in a study in HIV-negative women at a colposcopy clinic in Brazil (18.2%).14 However, the prevalence of CIN among women who reported more than 50 partners over their lifetime in our study was significantly higher (33%), and even higher than women with CD4 < 200/mm³ (42%), although HIV-associated immunosuppression is known to alter the relative carcinogenicity of HR-HPV types.27

A high prevalence of prior STIs (59.2%) was found in this study at a rate similar to that found in a study in the city of São Paulo, Brazil, in which the prevalence of was STIs around 61% in a group of women living with AIDS.12 Among drug users, the prevalence of STIs reached 73.0%. In the present study, the prevalence of STIs was also exceedingly high in the age group between 35 and 50 years (69.0%) and among women with more than 20 partners (72.7%). Although several low-income countries have achieved WHO targets for eliminating congenital syphilis, increased rates of this STI in HIV-infected people is a strong reminder of the tenacity of Treponema pallidum infection.31 The prevalence of syphilis was higher in women who had not received HAART (18.5%) and among women with detectable viral load (14.3%). In a cohort study of 2410 patients in Switzerland, from 1995 to 1997, the incidence of opportunistic infections decreased from 15.1 per 100 person-years in the six months before initiating HAART to 7.7 and 2.6 per 100 person-years in the first three and six months after starting HAART, respectively.32

The many limitations and challenges of implementing treatment as prevention should be pointed out to emphasize that sustained, population-level prevention benefit from earlier and wider use of HAART. It is important to highlight that HAART does not prevent other STIs and can give a false idea of complete protection.

A high prevalence of STIs was observed among HIV-infected women in our investigation. Most patients were on HAART and only 5% of them had a CD4 count <200 cells/mm3. However, more than half of the women were diagnosed with at least one STI at the first medical visit and reported unprotected sex.

Prevention programs need to focus on counseling for WLHIV and their regular partners with interventions such as couple counseling and education programs. Improved cervical cancer screening is urgent to prevent the expected increase in invasive cervical cancer among HIV-infected women with improved life expectancy as a result of HAART.