Search tips
Search criteria 


Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Sex Transm Infect. Author manuscript; available in PMC 2013 September 1.
Published in final edited form as:
PMCID: PMC3748151

Trichomoniasis and HIV interactions: a review



To discuss the epidemiology of Trichomonas vaginalis (TV) and HIV co-infections, the role of TV in acquisition and transmission of HIV, special treatment considerations for TV among women with HIV and the prevention of TV among HIV-infected persons.


Systematic review.

Data source

Review of literature of EMBASE and PubMed databases from January 1990 to February 2013. Search keywords included TV, HIV co-infections, HIV acquisition, HIV transmission, HIV shedding, TV treatment, HIV and couples studies.

Review method

We included studies of any design that contained the selected search words and were published during the specified time frame. We then searched the reference lists of included papers for additional papers and included these when relevant.


There is strong evidence that TV increases both transmission and acquisition of HIV among women, and that successful treatment for TV can reduce HIV genital shedding. Single dose metronidazole (MTZ) should no longer be used for HIV+ women with TV given the high rates of asymptomatic bacterial vaginosis co-infections and other factors that may render MTZ less effective in HIV+ women. Prevention of TV among HIV+ persons is similar to among HIV, including promotion of condoms as well as regular screening and prompt treatment. There may be a role for expedited partner treatment for the prevention of repeat infections, but most repeat infections are clinical treatment failures. Diligence in screening and treating TV among both HIV− susceptible and HIV+ persons is an important public health strategy.

Trichomonas vaginalis (TV) is the most common non-viral sexually transmitted infection (STI) worldwide1 and has been associated with pelvic inflammatory disease and adverse pregnancy outcomes.2 Once thought to be a minor STI, TV is now being given more attention because of its potential role in both the acquisition36 and transmission79 of HIV. In this paper, we discuss the epidemiology of HIV and TV co-infections, present evidence that TV plays a role in HIV acquisition and HIV transmission, describe the theories of how TV amplifies HIV transmission, discuss issues of TV treatment among HIV positive women, and present potential prevention measures of TV among HIV+ persons.


EMBASE and PubMed databases were searched with date ranges between January 1990 and February 2013. Search words included: TV and HIV acquisition, TV and HIV transmission, HIV shedding, epidemiology of HIV/TV co-infections, modelling and TV treatment and HIV, and TV and HIV and couples studies.

Selection of papers for review

The review of papers was completed by two reviewers (PK and AA). Titles and abstracts (where abstracts were available) were screened for relevance and duplicates removed. Relevant papers were reviewed for the association between TV and HIV acquisition, TV and HIV transmission (mostly via genital shedding), and HIV shedding and TV treatment. Reference lists of relevant papers were also searched and any additional relevant studies from these lists were included.


Using all search terms in both databases, 1068 papers were identified. After eliminating duplicates 560 remained. The titles and abstracts of these papers were reviewed for relevance and 33 papers were reviewed in full. An additional three studies on TV and HIV modelling and two abstracts were found on the topic of TV treatment among HIV+ women, and 40 other papers were found on TV/HIV co-infections and other related topics.

Epidemiology of TV and HIV co-infections

While the global prevalence of TV is unknown, rates differ by population and by region. TV disproportionately affects women of African descent. In the USA, the highest prevalence of TV is seen among African Americans with rates ranging from 13% to 51%,10 a rate well above the US population-based prevalence of 3%.3 African Americans are also the demographic group which also has the highest rate of HIV in the USA.4 Worldwide, the majority of the 174 million new cases of TV each year are found in Sub-Saharan Africa, a place where the majority of HIV infections also occur.5 In Sub-Saharan Africa, the rate of TV ranges from 11%6,7 in population-based studies to 20.9% in pregnant women,8 but selected cohorts have demonstrated much higher rates.

Women who have HIV have high rates of TV and women who have TV have excess rates of HIV. Prevalence of TV ranges from 6.1% to 52.5%8,9,1116 among HIV-positive women compared with 3.2%–34% among HIV-negative women.5,17

TV and HIV acquisition

There were 14 studies that examined the association between TV infection and HIV acquisition and all of them found a positive association, 11 of which were statistically significant. Of these studies, nine were cohort, two were nested case-control and three were partner study designs (two cohort and one nested case-control designs). Most of these studies used either wet prep or culture as the diagnostic test for TV, which have lower sensitivity than amplification methods and would likely have under-represented asymptomatic women. All three of the studies that used nucleic acid amplification techniques found statistically significant elevated risk for TV infection and a subsequent HIV infection.

It is possible that TV may just be a marker of some other factor that causes HIV infection. However, all three of the sero-discordant partner studies, the strongest of the study designs for examining this issue, demonstrated positive associations. Two did not achieve statistical significance likely because they were underpowered (n=415 and n=90). Table 1 presents details of the studies and figure 1 presents the effect measures and their 95% CI.

Figure 1
Trichomonas and HIV acquisition.
Table 1
Trichomonas and HIV acquisition

Using some of these studies as inputs, epidemiological modelling has demonstrated the potential role of TV on HIV transmission using data from the USA. Using population attributable risk curves, Sorvillo et al demonstrated that if TV amplifies HIV transmission twofold, as has been shown in some studies,25,27 and the prevalence of TV in a community is 25%, a rate commonly found among African American women studied, a fifth (20%) of HIV transmission in that population would be attributable to TV.31 This finding suggests that TV control may have an impact on the HIV-related disparities among African Americans in the USA. Quinlivan et al found similar findings. They estimated that 23% of the HIV transmission events from HIV-infected women may be attributable to TV infection when 22% of women are co-infected with TV, suggesting the importance of TV control among HIV+ women. 32 Chesson et al estimated that, in the USA, 747 new HIV cases a year in women are a result of the facilitative effects of TV on the transmission of HIV,33 proposing that TV control may be a cost savings initiative.

TV and HIV shedding

HIV shedding in the genital tract can theoretically increase the chance of HIV transmission; however, the amount of HIV needed for transmission to occur is unknown. Unlike TV and HIV acquisition, the association of TV on HIV genital shedding is less clear. There were 14 original studies (including one discordant partner study), one meta-analysis and one review paper that examined TV and HIV genital shedding. Of the 14 studies, over half (n=8) found an increased risk. The meta-analysis/review papers were also mixed. Many of these studies had small sample sizes and did not control for several key confounding variables, which could account for the variability in findings. Genital shedding of HIV, particularly among women, can be influenced by several factors. Among these factors are: plasma viral load, antiretroviral therapy (ART) status, other STIs, vaginal douching and unprotected sex with an HIV+ person. Therefore, studies of genital shedding must be adequately powered and well designed to reduce this potential confounding.

Other cofactors may increase TV-associated genital shedding. In a cohort of HIV+ women in New Orleans, USA, bacterial vaginosis (BV) seemed to act synergistically with TV to increase genial shedding. In this study, the odds of shedding HIV vaginally in the presence of TV alone, BV alone and TV/BV co-occurrence were 4.07 (95% CI 1.78 to 9.37), 5.65 (95% CI 2.64 to 12.01) and 18.63 (95% CI 6.71 to 51.72) respectively when compared with women with no diagnosis of TV or BV and adjusted for age, ART status and plasma viral load.34 The vaginal ecology may play an important role in sexual acquisition and transmission of HIV.

And while there is mounting evidence that ART status may be one of the most important preventive measures to reduce HIV genital shedding and consequently HIV transmission, there is evidence that even if plasma HIV is well controlled, HIV may still be expressed in genital fluids.35 Thus, measures to further reduce transmission beyond ART provision are needed. Table 2 presents details of the studies and figure 2 presents the effect measures and their 95% CI.

Figure 2
Trichomonas and HIV genital shedding. *The findings of Hobbs39 and Price42 are not shown in the figure because they did not present effect measures.
Table 2
Trichomonas and HIV genital shedding

While the association of TV infection on HIV genital shedding among HIV+ person has not been consistent, there is good evidence that TV treatment reduces HIV genital shedding. Five studies were reported in the literature and, of these, four found a decrease in HIV genital shedding after TV treatment. The one study that did not find an association had a sample size of 31. Two prospective studies in Africa 50,51 where women were not receiving ART, and one study in the USA where about half of the women were receiving ART45 found that HIV genital shedding decreased after TV treatment, suggesting a role for TV treatment in HIV prevention beyond ART provision. These findings may not be generalized to men since there are far fewer studies of both acquisition and transmission among men (see table 3).

Table 3
TV treatment and HIV shedding

Potential mechanisms whereby HIV amplifies HIV transmission

There are several possible mechanisms by which TV can increase susceptibly to HIV-1 including the aberrations caused by the inflammatory process, disruption of the mechanical barrier and impaired immune response.53 TV infection typically elicits an aggressive local cellular immune response with inflammation of the vaginal epithelium and exocervix in women and the urethra of men.10 The normal flora and pH are altered, producing a conducive environment for HIV-1 to pass through the cervicovaginal epithelium and mucosa infecting the host immune system.

TV may also increase the risk of HIV-1 acquisition by increasing susceptibility to BV or persistence of abnormal vaginal flora. When the normal flora of the vagina is disturbed there is a decrease in the proportion of H2O2 producing lactobacillus, which function to maintain a low vaginal pH.54 Without H2O2 producing lactobacillus the pH of the vaginal mucosa rises and pathogens that could not otherwise survive can now flourish. Decreased proportions of H2O2 producing lactobacillus and increased proportion of anaerobes have been associated in women infected with TV.55,56 In in vitro studies, lactic acid from all species of lactobacilli and H2O2 producing species have shown virucidal properties.57

An intact vaginal multilayered squamous epithelium provides a natural barrier to infection, as it does not appear to be susceptible to endocytosis and transcytosis of the HIV-1 virons. HIV-1 has been shown to pass though the thin gaps between squamous epithelial cells which could bring the virus into contact with CD4 T lymphocytes and Langerhans cells.58 Microabrasions caused during sexual intercourse removes the surface of the epithelium exposing the basal and stroma layers, weakening the barrier protection. TV frequently causes punctuate mucosal haemorrhages, which potentially compromises the mechanical barrier to infection. The epithelium of the cervicovaginal tissue is also disrupted by TV leading to the characteristic colpitis macularis, ‘strawberry cervix’ appearance and friability.59 These breaks in the surface epithelium facilitate the entry of HIV-1.

Vaginal innate mucosal immunity can become suppressed in the presence of TV. The main effector molecules of the innate mucosal immunity are cationic antimicrobial polypeptides, including secretory leukoprotease inhibitor (SLPI) and human B defensins, which work by downregulating inflammatory responses of macrophages and monocytes.60 It has been reported that SLPI has virucidal properties against HIV-1 in vitro.60 TV has been shown to decrease SLPI and other innate immune factors.61 The suppressed innate immunity can also allow other pathogens to flourish. There is some evidence that there may be some non-infectious causes of inflammation that increase cervicovaginal HIV-1 shedding.

TV induces a clinical or subclinical pro-inflammation of the cervix and vaginal tissues. Inflammation is a protective reaction in response to infections from vaginal pathogens.62 Women who are infected with TV show increased levels of neutrophils, interleukin 1B (IL-1B), IL-8 and macrophage inflammatory protein three α (MIP-3α), which are markers of a pro-inflammatory response.62,63 Langerhans-like CD34 progenitor dendritic cells are effective antigen presenting cells that are recruited to the vaginal mucosal surface by the chemokine MIP-3α.63 Macrophages, dendritic cells, and CXC4 and CCR5 expressing T lymphocytes are densely located in the subepithelia stromal tissues in the vagina. HIV most likely uses CD4/CCR5 intraepithelia cells, such as lymphocytes and Langerhans, to cross the mucosal surface and infect CD4 T lymphocytes.64 The inflammatory response induces the recruitment of leukocytes including HIV target cells such as CD4 bearing lymphocytes and macrophages to which HIV can bind and gain access. By activating the inflammation pathways and mediators, HIV target cells are localised to the site of inflammation. This facilitates the uptake of the viral particles and subsequent infection.

TV treatment issues among HIV positive women

Treatment of TV with single dose metronidazole (MTZ) is imperfect. High repeat infection rates (8%–20%6570) among women receiving 2 g dose of MTZ for the treatment of TV have brought into question the effectiveness of single dose treatment.

In a study of HIV−/TV+ women who were given directly observed single dose MTZ and provided with medication to deliver to their sex partner(s), repeat infections rates were high (8%) and nearly all (92%) were attributed to clinical treatment failure,11 suggesting that clinical failure is the reason for lack of efficacy of single dose MTZ.

Re-infection from an untreated partner is another potential source of repeat infections. Patient-delivered partner treatment (PDPT), or the provision of antibiotics to infected index persons to deliver to their sex partners, is a possible alternative to the standard of partner referral or telling the index woman to refer her partner for care. While PDPT has been found to be superior to standard partner referral methods for reducing repeat Chlamydia trachomatis and Neisseria gonorrhoeae infections,24 the efficacy of PDPT for TV is less clear. Two published randomised controlled trials (RCTs) of PDPT for TV given to index women to deliver to their male sex partners found conflicting results.13,25 However, these studies were single centred and likely underpowered, and thus larger multi-centred trials are needed. One study of HIV+/TV+ women demonstrated high adherence to PDPT71 suggesting that, while Centers for Disease Control and Prevention have not yet recommended PDPT for HIV+ women, it may be a feasible option.

Repeat infection rates appear to be particularly high among HIV+ women ranging from 18.3% to 36.9%,13,66,72 suggesting that some factors specific to HIV+ women may be interfering with single dose MTZ therapy. A recently completed RCT among HIV-infected women with TV found multi-dose MTZ to be superior to single dose treatment.22 This RCT also found that the presence of BV was likely a major factor in the early failure of the single dose treatment.73 Another study corroborated these findings and found that women who were receiving nevirapine-containing ART had higher rates of treatment failure74 Subsequent analysis of the US-based study also found that ART interfered with MTZ treatment of TV.75 These studies suggest that ART may reduce the efficacy of MTZ. There are also data indicating that BV may play a factor in MTZ treatment failure.73

The Centers for Disease Control and Prevention guidelines for treatment of TV include: MTZ or tinidazole 2 g single dose as the recommended regimens, and MTZ 500 mg twice daily 7 day dose as the alternative treatment regimen, but suggest that for HIV+ women the multi-dose therapy can be considered.21

Prevention of TV

Prevention of TV for HIV+ persons is similar to those for HIV− persons. Primary prevention includes promotion of condoms and other safer sex activities to reduce the chance of exposure. There is some evidence that nonoxynol-9 can be used as an anti-trichomonal agent;76 thus, condoms that contain nonoxynol-9 may also serve to prevent trichomonal infections. Secondary prevention includes screening and prompt treatment. Periodic presumptive treatment among female sex workers in Papua New Guinea demonstrated a twofold decrease in TV.77 Increased use of improved diagnostics in women is needed.

Since TV testing for men is difficult and the majority of TV-infected men are asymptomatic,78 partner treatment is paramount to reducing early repeat infections in women. Clinicians should consider diagnosis and treatment of TV in men. The influence of male circumcision on incident TV has demonstrated both protective effects among men and women79 and no effect among men.80


The evidence is clear that TV is associated with HIV acquisition among women. And while less clear that it is associated with increased genital shedding of HIV among HIV+ persons, it is clear that TV treatment reduces vaginal shedding. While it is unknown how much genital HIV is needed to transmit HIV, we do know that it is a necessary, but not sufficient, factor and evidence is mounting that while ART can significantly reduce plasma viral loads, there may be reservoirs of genital HIV and this could increase transmission.

Given the high rates of TV in populations in HIV vulnerable populations and among HIV+ persons, TV should be given higher priority for STD control programmes. At a minimum, HIV susceptible women in areas with high rates of HIV should be screened for TV. In addition, HIV+ women should be consistently screened and treated with multi-dose MTZ to prevent the possibility of perinatal and sexual HIV transmission.

Key messages

  • [triangle] There is strong evidence that Trichomonas vaginalis (TV) increases both transmission and acquisition of HIV among women, and thus diligence in screening and treating TV among HIV susceptible and HIV+ women is an important public health strategy.
  • [triangle] Treatment of TV among HIV+ women may require multi-dose of metronidazole given the high rates of asymptomatic bacterial vaginosis co-infections, changes in vaginal ecology and impaired immunity of HIV+ women that may interfere with single dose treatment.
  • [triangle] Prevention of TV among HIV+ women is similar to HIV− persons, but special attention should be paid to prevent recurrent infections which are highly prevalent among HIV+ women.


Funding Funding for this review paper was from NIAID 1R01AI097080-01A1.


Contributors PK and AA designed the study, conducted the literature search and evaluated the papers.

Competing interests None.

Provenance and peer review Commissioned; externally peer reviewed.


1. World Health Organization W . Prevalence and incidence of selected sexually transmitted infections, Chlamydia trachomatis, Neisseria gonorrhoeae, syphlis and Trichomonas vaginalis: methods and results used by WHO to generate 2005 estimates. Geneva, Switzerland: 2011.
2. Hobbs MM, Sena A, Swygard H, et al. Trichomons vaginalis and trichomoniasis. In: Holmes KK, Stamm WE, Piot P, et al., editors. Sexually transmitted diseases. 4th edn. McGraw-Hill; New York: 2008. pp. 771–94.
3. Sutton M, Sternberg M, Koumans EH, et al. The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001–2004. Clin Infect Dis. 2007;45:1319–26. [PubMed]
4. Centers for Disease Control and P . HIV among African Americans. National Center for HIV/AIDS VH, STD, and TB Prevention; Atlanta: 2011.
5. Johnston VJ, Mabey DC. Global epidemiology and control of Trichomonas vaginalis. Curr Opin Infect Dis. 2008;21:56–64. [PubMed]
6. Watson-Jones D, Mugeye K, Mayaud P, et al. High prevalence of trichomoniasis in rural men in Mwanza, Tanzania: results from a population based study. Sex Transm Infect. 2000;76:355–62. [PMC free article] [PubMed]
7. Klinger EV, Kapiga SH, Sam NE, et al. A Community-based study of risk factors for Trichomonas vaginalis infection among women and their male partners in Moshi urban district, northern Tanzania. Sex Transm Dis. 2006;33:712–8. [PubMed]
8. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin a deficiency, and other risk factors for shedding of HIV-1 infected cells from the cervix and vagina. Lancet. 1997;350:922–7. [PubMed]
9. McClelland RS, Sangare L, Hassan WM, et al. Infection with Trichomonas vaginalis increases the risk of HIV-1 acquisition. J Infect Dis. 2007;195:698–702. [PubMed]
10. Shafir SC, Sorvillo FJ, Smith L. Current issues and considerations regarding trichomoniasis and human immunodeficiency virus in African-Americans. Clin Microbiol Rev. 2009;22:37–45. Table of Contents. [PMC free article] [PubMed]
11. Brogly SB, Watts DH, Ylitalo N, et al. Reproductive health of adolescent girls perinatally infected with HIV. Am J Public Health. 2007;97:1047–52. [PubMed]
12. Cu-Uvin S, Ko H, Jamieson DJ, et al. Prevalence, incidence, and persistence or recurrence of trichomoniasis among human immunodeficiency virus (HIV)-positive women and among HIV-negative women at high risk for HIV infection. Clin Infect Dis. 2002;34:1406–11. [PubMed]
13. Magnus M, Clark R, Myers L, et al. Trichomonas vaginalis among HIV-Infected women: are immune status or protease inhibitor use associated with subsequent T. vaginalis positivity? Sex Transm Dis. 2003;30:839–43. [PubMed]
14. Miller M, Liao Y, Wagner M, et al. HIV, the clustering of sexually transmitted infections, and sex risk among African American women who use drugs. Sex Transm Dis. 2008;35:696–702. [PubMed]
15. Moodley P, Wilkinson D, Connolly C, et al. Influence of HIV-1 coinfection on effective management of abnormal vaginal discharge. Sex Transm Dis. 2003;30:1–5. [PubMed]
16. Watts DH, Springer G, Minkoff H, et al. The occurrence of vaginal infections among HIV-infected and high-risk HIV-uninfected women: longitudinal findings of the women's interagency HIV study. J Acquir Immune Defic Syndr. 2006;43:161–8. [PubMed]
17. Kalichman SC, Pellowski J, Turner C. Prevalence of sexually transmitted co-infections in people living with HIV/AIDS: systematic review with implications for using HIV treatments for prevention. Sex Transm Infect. 2011;87:183–90. [PubMed]
18. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: results from a cohort study. Aids. 1993;7:95–102. [PubMed]
19. Laga M, Alary M, Nzila N, et al. Condom promotion, sexually transmitted diseases treatment, and declining incidence of HIV-1 infection in female Zairian sex workers. Lancet. 1994;344:246–8. [PubMed]
20. Taha TE, Hoover DR, Dallabetta GA, et al. Bacterial vaginosis and disturbances of vaginal flora: association with increased acquisition of HIV. Aids. 1998;12:1699–706. [PubMed]
21. Ghys PD, Diallo MO, Ettiegne-Traore V, et al. Effect of interventions to control sexually transmitted disease on the incidence of HIV infection in female sex workers. AIDS. 2001;15:1421–31. [PubMed]
22. Myer L, Denny L, de Souza M, et al. Distinguishing the temporal association between women's intravaginal practices and risk of human immunodeficiency virus infection: a prospective study of South African women. Am J Epidemiol. 2006;163:552–60. [PubMed]
23. Kleinschmidt I, Rees H, Delany S, et al. Injectable progestin contraceptive use and risk of HIV infection in a South African family planning cohort. Contraception. 2007;75:461–7. [PubMed]
24. Van Der Pol B, Kwok C, Pierre-Louis B, et al. Trichomonas vaginalis infection and human immunodeficiency virus acquisition in African women. J Infect Dis. 2008;197:548–54. [PubMed]
25. Mavedzenge SN, Pol BV, Cheng H, et al. Epidemiological synergy of Trichomonas vaginalis and HIV in Zimbabwean and South African women. Sex Transm Dis. 2010;37:460–6. [PubMed]
26. Delany-Moretlwe S, Nanoo A, Nagpal A, et al. Risk factors associated with HIV acquisition: a comparative analysis of older and younger women who participated in the MDP301 trial in Johannesburg. Sex Transm Infect. 2011;87:A179–80.
27. Vandepitte J, Weiss HA, Bukenya J, et al. Alcohol use, mycoplasma genitalium, and other STIs sssociated with HIV incidence among women at high risk in Kampala, Uganda. J Acquir Immune Defic Syndr. 2013;62:119–26. [PMC free article] [PubMed]
28. Quinn TC, Wawer MJ, Sewankambo N, et al. Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group. N Engl J Med. 2000;342:921–9. [PubMed]
29. Hester RA, Kennedy SB. Candida infection as a risk factor for HIV transmission. J Womens Health (Larchmt) 2003;12:487–94. [PubMed]
30. Hughes JP, Baeten JM, Lingappa JR, et al. Determinants of per-coital-act HIV-1 infectivity among African HIV-1-serodiscordant couples. J Infect Dis. 2012;205:358–65. [PMC free article] [PubMed]
31. Sorvillo F, Smith L, Kerndt P, et al. Trichomonas vaginalis, HIV, and African-Americans. Emerg Infect Dis. 2001;7:927–32. [PMC free article] [PubMed]
32. Quinlivan EB, Patel SN, Grodensky CA, et al. Modeling the impact of Trichomonas vaginalis infection on HIV transmission in HIV-infected individuals in medical care. Sex Transm Dis. 2012;39:671–7. [PMC free article] [PubMed]
33. Chesson HW, Blandford JM, Pinkerton SD. Estimates of the annual number and cost of new HIV infections among women attributable to trichomoniasis in the United States. Sex Transm Dis. 2004;31:547–51. [PubMed]
34. Fastering D KP. Vaginal Shedding of HIV-1 RNA in the presence of Trichomonas vaginalis and bacterial vaginosis.. 19th International AIDS Conference; Washington D.C. USA. 2012.
35. Baggaley RF, White RG, Hollingsworth TD, et al. Heterosexual HIV-1 infectiousness and antiretroviral use: systematic review of prospective studies of discordant couples. Epidemiology. 2013;24:110–21. [PubMed]
36. Clemetson DB, Moss GB, Willerford DM, et al. Detection of HIV DNA in cervical and vaginal secretions. Prevalence and correlates among women in Nairobi, Kenya. JAMA. 1993;269:2860–4. [PubMed]
37. Ghys PD, Fransen K, Diallo MO, et al. The associations between cervicovaginal HIV shedding, sexually transmitted diseases and immunosuppression in female sex workers in Abidjan, Cote d'Ivoire. AIDS. 1997;11:F85–93. [PubMed]
38. John GC, Nduati RW, Mbori-Ngacha D, et al. Genital shedding of human immunodeficiency virus type 1 DNA during pregnancy: association with immunosuppression, abnormal cervical or vaginal discharge, and severe vitamin A deficiency. J Infect Dis. 1997;175:57–62. [PMC free article] [PubMed]
39. Hobbs MM, Kazembe P, Reed AW, et al. Trichomonas vaginalis as a cause of urethritis in Malawian men. Sex Transm Dis. 1999;26:381–7. [PubMed]
40. Kovacs A, Wasserman SS, Burns D, et al. Determinants of HIV-1 shedding in the genital tract of women. Lancet. 2001;358:1593–601. [PubMed]
41. Spinillo A, Debiaggi M, Zara F, et al. Factors associated with nucleic acids related to human immunodeficiency virus type 1 in cervico-vaginal secretions. BJOG : an international journal of obstetrics and gynaecology. 2001;108:634–41. [PubMed]
42. Price MA, Zimba D, Hoffman IF, et al. Addition of treatment for trichomoniasis to syndromic management of urethritis in Malawi: a randomized clinical trial. Sex Transm Dis. 2003;30:516–22. [PubMed]
43. Cu-Uvin S, Snyder B, Harwell JI, et al. Association between paired plasma and cervicovaginal lavage fluid HIV-1 RNA levels during 36 months. J Acquir Immune Defic Syndr. 2006;42:584–7. [PubMed]
44. Neely MN, Benning L, Xu J, et al. Cervical shedding of HIV-1 RNA among women with low levels of viremia while receiving highly active antiretroviral therapy. J Acquir Immune Defic Syndr. 2007;44:38–42. [PMC free article] [PubMed]
45. Kissinger P, Amedee A, Clark RA, et al. Trichomonas vaginalis treatment reduces vaginal HIV-1 shedding. Sex Transm Dis. 2009;36:11–6. [PMC free article] [PubMed]
46. Paz-Bailey G, Sternberg M, Puren AJ, et al. Determinants of HIV type 1 shedding from genital ulcers among men in South Africa. Clin Infect Dis. 2010;50:1060–7. [PubMed]
47. Tanton C, Weiss HA, Le Goff J, et al. Correlates of HIV-1 genital shedding in Tanzanian women. PloS one. 2011;6:e17480. [PMC free article] [PubMed]
48. Johnson LF, Lewis DA. The effect of genital tract infections on HIV-1 shedding in the genital tract: a systematic review and meta-analysis. Sex Transm Dis. 2008;35:946–59. [PubMed]
49. Rottingen JA, Cameron DW, Garnett GP. A systematic review of the epidemiologic interactions between classic sexually transmitted disease and HIV: how much really is known? Sex Trans Dis. 2001;20:579–97. [PubMed]
50. Anderson BL, Firnhaber C, Liu T, et al. Effect of trichomoniasis therapy on genital HIV viral burden among African women. Sex Transm Dis. 2012;39:638–42. [PMC free article] [PubMed]
51. Wang CC, McClelland RS, Reilly M, et al. The effect of treatment of vaginal infections on shedding of human immunodeficiency virus type 1. J Infect Dis. 2001;183:1017–22. [PubMed]
52. Masese LN, Graham SM, Gitau R, et al. A prospective study of vaginal trichomoniasis and HIV-1 shedding in women on antiretroviral therapy. BMC infectious diseases. 2011;11:307. [PMC free article] [PubMed]
53. Thurman AR, Doncel GF. Innate immunity and inflammatory response to Trichomonas vaginalis and bacterial vaginosis: relationship to HIV acquisition. American Journal of Reproductive Immunology. 2011;65:89–98. [PubMed]
54. Hawes SE, Hillier SL, Benedetti J, et al. Hydrogen peroxide-producing lactobacilli and acquisition of vaginal infections. J Infect Dis. 1996;174:1058–63. [PubMed]
55. Brotman RM, Bradford LL, Conrad M, et al. Association between Trichomonas vaginalis and vaginal bacterial community composition among reproductive-age women. Sex Transm Dis. 2012;39:807–12. [PMC free article] [PubMed]
56. Baeten JM, Hassan WM, Chohan V, et al. Prospective study of correlates of vaginal Lactobacillus colonisation among high-risk HIV-1 seronegative women. Sex Transm Infect. 2009;85:348–53. [PMC free article] [PubMed]
57. Klebanoff SJ. Coombs R Viricidal effect of Lactobacillus acidophilus on human immunodeficiency virus type 1: possible role in heterosexual transmission. The Journal of experimental medicine. 1991;174:289–92. [PMC free article] [PubMed]
58. Hladik F, Hope TJ. HIV infection of the genital mucosa in women. Current HIV/AIDS reports. 2009;6:20–8. [PubMed]
59. Swygard H, Sena AC, Hobbs MM, et al. Trichomoniasis: clinical manifestations, diagnosis and management. Sex Transm Infect. 2004;80:91–5. [PMC free article] [PubMed]
60. McNeely TB, Dealy M, Dripps DJ, et al. Secretory leukocyte protease inhibitor: a human saliva protein exhibiting anti-human immunodeficiency virus 1 activity in vitro. The Journal of clinical investigation. 1995;96:456–64. [PMC free article] [PubMed]
61. Draper D, Donohoe W, Mortimer L, et al. Cysteine proteases of Trichomonas vaginalis degrade secretory leukocyte protease inhibitor. J Infect Dis. 1998;178:815–9. [PubMed]
62. Cauci S, Culhane JF. Modulation of vaginal immune response among pregnant women with bacterial vaginosis by Trichomonas vaginalis Chlamydia trachomatis Neisseria gonorrhoeae, and yeast. Am J Obstet Gynecol. 2007;196:133, e1–7. [PubMed]
63. Fichorova RN, Trifonova RT, Gilbert RO, et al. Trichomonas vaginalis lipophosphoglycan triggers a selective upregulation of cytokines by human female reproductive tract epithelial cells. Infection and immunity. 2006;74:5773–9. [PMC free article] [PubMed]
64. Shattock RJ, Haynes BF, Pulendran B, et al. Improving defences at the portal of HIV entry: mucosal and innate immunity. PLoS medicine. 2008;5:e81. [PMC free article] [PubMed]
65. Schwebke JR, Desmond RA. A randomized controlled trial of partner notification methods for prevention of trichomoniasis in women. Sex Transm Dis. 2010;37:392–6. [PubMed]
66. Kissinger P, Secor WE, Leichliter JS, et al. Early repeated infections with Trichomonas vaginalis among HIV-positive and HIV-negative women. Clin Infect Dis. 2008;46:994–9. [PubMed]
67. Krashin JW, Koumans EH, Bradshaw-Sydnor AC, et al. Trichomonas vaginalis prevalence, incidence, risk factors and antibiotic-resistance in an adolescent population. Sex Transm Dis. 2010;37:440–4. [PubMed]
68. Tidwell BH, Lushbaugh WB, Laughlin MD, et al. A double-blind placebo-controlled trial of single-dose intravaginal versus single-dose oral metronidazole in the treatment of trichomonal vaginitis. J Infect Dis. 1994;170:242–6. [PubMed]
69. Spence MR, Harwell TS, Davies MC, et al. The minimum single oral metronidazole dose for treating trichomoniasis: a randomized, blinded study. Obstet Gynecol. 1997;89:699–703. [PubMed]
70. duBouchet L, Spence MR, Rein MF, et al. Multicenter comparison of clotrimazole vaginal tablets, oral metronidazole, and vaginal suppositories containing sulfanilamide, aminacrine hydrochloride, and allantoin in the treatment of symptomatic trichomoniasis. Sex Transm Dis. 1997;24:156–60. [PubMed]
71. Gatski M, Mena L, Levison J, et al. Patient-delivered partner treatment and Trichomonas vaginalis repeat infection among human immunodeficiency virus-infected women. Sex Transm Dis. 2010;37:502–5. [PMC free article] [PubMed]
72. Niccolai LM, Kopicko JJ, Kassie A, et al. Incidence and predictors of reinfection with Trichomonas vaginalis in HIV-infected women. Sex Transm Dis. 2000;27:284–8. [PubMed]
73. Gatski M, Martin DH, Levison J, et al. The influence of bacterial vaginosis on the response to Trichomonas vaginalis treatment among HIV-infected women. Sex Transm Infect. 2011;87:205–8. [PMC free article] [PubMed]
74. Balkus JE, Richardson BA, Kiarie J, et al. Infectious Diseases Society of Obstetrics and Gynecology. Whistler, Canada: 2012. Nevirapine-based antiretroviral therapy is associated with an increased risk of treatment failure of single-dose 2g oral metronidazole for trichomonas vaginalis infection.
75. Kissinger P, Adamski A, Clark RA, et al. Does antiretroviral therapy interfere with the treatment of Trichomonas vaginalis among HIV+ women? Sex Trans Dis. 2013 in press. [PMC free article] [PubMed]
76. Jain A, Lal N, Kumar L, et al. Novel trichomonacidal spermicides. Antimicrob Agents Chemother. 2011;55:4343–51. [PMC free article] [PubMed]
77. Cudmore SL, Garber GE. Prevention or treatment: the benefits of Trichomonas vaginalis vaccine. Journal of infection and public health. 2010;3:47–53. [PubMed]
78. Sobel JD. What's new in bacterial vaginosis and trichomoniasis? Infectious disease clinics of North America. 2005;19:387–406. [PubMed]
79. Weiss HA, Dickson KE, Agot K, et al. Male circumcision for HIV prevention: current research and programmatic issues. Aids. 2010;24(Suppl 4):S61–9. [PubMed]
80. Mehta SD, Moses S, Agot K, et al. Adult male circumcision does not reduce the risk of incident Neisseria gonorrhoeae, Chlamydia trachomatis, or Trichomonas vaginalis infection: results from a randomized, controlled trial in Kenya. J Infect Dis. 2009;200:370–8. [PMC free article] [PubMed]