STD surveillance was recognised as a useful comparison of HIV risk assessment, .. J. The interrelationship of sexually transmitted diseases and HIV infection: Rapid control of chancroid in a South African mining company [abstract ]. Other viral infections, such as herpes simplex virus type 2 (causing genital ulcer) Individuals with HIV infection are also more likely to transmit the infection to. Having a sexually transmitted disease (STD) can increase your HIV risk by According to the latest research, HIV-positive people on STD.
In the accompanying editorial, Glynn and colleagues update an earlier meta-analysis of prevalent HSV-2 on incident HIV, and find similar estimates. These and other findings suggest that prevalent HSV-2 increases the risk of acquisition of HIV, but HSV-2 can also increase the risks of transmission from dually infected people.
The reduction in HIV viral load is significant, at around 0. Acyclovir was given to the dually infected partner, and the outcome was transmission to the discordant partner.
Interpreting these trials has been challenging, and it is important not to conclude that the intervention is ineffective before questioning whether the intervention could be improved. Similarly, it is worth considering whether the failure to show a reduction in HIV acquisition or transmission due to poor drug adherence, noted in one study [ 35 ], although this did not appear to be a factor in the other two trials. Some have suggested that the drug dosage may have been too low, and there is evidence that acyclovir mg or valacyclovir mg twice daily produce greater viral suppression.
These trials, although very large, may still have been underpowered, particularly if the PAR is relatively small and, as some authors commented,[ 38 ] the inclusion of counselling and condoms to both arms of the study meant that the incidence was lower than expected.
Conclusion There is a clear association between bacterial and viral STI and the risk of HIV infection at both individual and population levels. It is highly probable that there is a causal link given the consistency of epidemiological data and the strong biological plausibility and clear mechanisms of effect.
The contribution of STIs to the sexual transmission of HIV
Why then have the trials of interventions been so disappointing? For each intervention there are many specific factors, ranging from individual level compliance through to population coverage.
The lack of effect of STI treatment trials at a population level may be due to the epidemic phase and specific local conditions. Further insights are suggested by mathematical modelling studies, although these are of course only as robust as the assumptions and parameter estimates on which they are based.
They can be helpful in exploring the potential impact of an effective intervention, and also the factors that may limit the findings of a specific trial.
The effectiveness of PPT was analysed in a mathematical model looking at female sex workers in Johannesburg, South Africa. It may be worth exploring whether suppressive therapy should be given to both partners in HIV-discordant but HSV-concordant couples. HSV-2 vaccination may have greater potential. However, models of the impact of HSV-2 vaccination on HIV transmission show that it would take many years to have any major impact on transmission even with quite high coverage.
Gray and Wawer have suggested it is time to reassess the importance of STI prevention as part of HIV programmes, arguing that given the lack of evidence of impact, resources should be shifted towards interventions of known efficacy. From the public health and service provision point of view, whether there is a causal association between concurrent STIs and HIV acquisition does not really matter as the mode of transmission and many of the risk factors are the same.
There are many advantages gained from incorporation of STI control into HIV programmes, or rather from providing a more integrated approach to preventive interventions for reproductive and sexually transmitted infections, of which HIV is just one.
Footnotes This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form.
Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Piot P, Laga M. Genital ulcers, other sexually transmitted diseases, and the sexual transmission of HIV. Female to male transmission of human immunodeficiency virus type 1: A systematic review of the epidemiologic interactions between classic sexually transmitted diseases and HIV: Sexual transmission of HIV Initial studies demonstrated that HSV-2 reactivation, with the presence of clinical lesions, was associated with transient increases in genital shedding and levels of plasma HIV-1 RNA [ 1425 ].
A small study by Schacker et al. Additional studies involving diverse HIV-1 populations are shown in Table 1. In the largest study to date, Celum et al. A randomized, crossover trial of two types and doses of antiherpetic medications was evaluated valacyclovir 1. Mean plasma HIV-1 levels were significantly lower in the valacyclovir compared with the acyclovir arm: This study suggested that higher doses of antiherpetic medications may offer greater benefit in reducing HIV-1 RNA levels and revealed no increase in adverse events using the higher dose.
Of note, characteristics associated with a larger decrease in HIV-1 viral load included older median age, valacyclovir use, and higher compliance rates [ 28 ]. The reduction in HIV-1 RNA loads by these agents is due to suppression of HSV-2 replication and its interaction with the HIV-1 virus, as described above, as well as the potential direct antiretroviral effects of acyclovir [ 29 — 31 ].
Further studies are needed to examine the benefit of antiherpetic medication on systemic HIV-1 control in this setting.
While these studies demonstrated that antiherpetic therapy reduces genital and plasma HIV-1 RNA levels among patients not receiving CART [ 814 — 21 ], whether this therapy could slow HIV-1 clinical progression was not specifically examined. A recent review noted that a reduction in HIV-1 viral load of 0. Additionally, during early trials of antiretroviral therapy ARTacyclovir was associated with increased survival [ 34 ].
Hence, clinical trials were undertaken to determine if the use of acyclovir could slow HIV-1 progression. Assuming that the incidence of endpoints remained constant over time, acyclovir would have delayed the median time to an endpoint by estimated Participants were randomized to acyclovir mg twice daily or placebo and followed for 24 months.
In addition to these studies [ 2324 ], one study evaluated the impact of acyclovir mg twice daily versus placebo on the viral load set point during early HIV-1 infection but found no significant effect [ 35 ]. Advantages of antiherpetic medication use in these settings include its low cost i.
Therapy is most advantageous when utilized continuously, since the interruption of therapy is associated with viral rebound [ 21 ]. The effect of antiherpetic medication on plasma HIV-1 concentrations can be seen within a week of initiation [ 21 ], with no reduction in efficacy noted over time [ 23 ].
The added value of antiherpetic medications concurrently with CART or in other clinical scenarios at time of seroconversion or among HIV-2 patients requires further evaluation.
- The link between sexually transmitted infections and HIV
- The contribution of STIs to the sexual transmission of HIV
Current evidence suggests that HIV-1 infection modifies the course of HBV with an adverse impact on HBV-related liver disease progression, including higher serum HBV DNA polymerase activity; lower rates of loss of serum hepatitis B e antigen HBeAg ; and increased risk of cirrhosis, liver-related mortality, and hepatocellular carcinoma, especially among patients with lower CD4 cell counts [ 3641 — 46 ]. Other studies, however, have shown a significant impact on ART outcomes [ 54 — 56 ].
HBV is thought to mediate destruction of CD4 cells through T-cell activation or splenic sequestration seen in advanced liver disease [ 53 ].
Other studies have not detected differences in CD4 cell counts prior to ART initiation [ 495467 ]. In one study, individuals with occult hepatitis B HBV DNA present in the absence of hepatitis B surface antigen demonstrated lower CD4 cell counts as compared to individuals without occult hepatitis B [ 68 ].
However, the studies by Law and Hawkins showed no difference by 48 weeks and borderline significance at 12 months, respectively [ 46555667 ]. In addition to the potential effects on CD4 cell counts, several studies have examined the impact of coinfection on the plasma HIV-1 viral load. Evaluation of HIV-1 viral load at ART initiation has not shown any differences, but there are conflicting data on virologic suppression, with some studies showing no differences in the proportion of individuals achieving virologic suppression over time [ 555765 — 67 ].
Nevertheless, all-cause mortality has been shown to be higher, most commonly attributable to liver-related deaths [ 424673 ].
Journal of Sexually Transmitted Diseases
A meta-analysis including 11 studies with 12, patients showed a significantly increased risk for all-cause mortality in coinfected patients [ 73 ]. The negative impact of HIV-1 infection on the natural history of HCV infection is well established; HCV-associated liver disease, including fibrosis, cirrhosis, and end-stage liver disease, is accelerated among HIVinfected populations.
For example, progression to cirrhosis is times higher in coinfected than monoinfected individuals, with a third of coninfected patients estimated to progress to cirrhosis in less than 20 years [ 77 ].
An increased risk of liver-related deaths among coinfected compared with HCV monoinfected drug users despite CART use has also been reported from a recent year prospective study [ 78 ]. In a meta-analysis of studies calculating the HIV per-act transmission risk during heterosexual intercourse, Marie-Claude Boily and colleagues found that the risk appeared to be greater in higher-income countries than in lower-income countries.What is The Difference Between HIV and AIDS?
One possible explanation of the divergence is to do with rates of sexually transmitted infections. The studies conducted in lower-income countries mainly in Africa indicated a much higher transmission risk. Furthermore, the risk appeared higher from women to men, the opposite way round to higher-income countries and less biologically plausible. The risk in lower-income countries from men to women was 1 per acts of intercourse and from women to men 1 per acts.
The authors suggested that the differences seen were caused by much higher rates of STI infection in lower-income countries, especially in men. The per-act transmission risk when one partner had genital-ulcer disease GUD was 2. GUD is a term that covers any visible external ulcer or sore, which can be caused by herpes, syphilis, chancroid, candida or several non-sexually transmitted conditions.
Ulcerative STIs, such as syphilis, herpes and chancroid, cause lesions on the genitals and anus that may serve as ports of entry or exit for HIV.