There have been fewer studies in women, compared to men,
examining the association between viral loads in the blood plasma with that in
the genital tract. However, most
studies that have looked at this suggest that viral load in blood and vaginal
secretions is usually strongly correlated, and that it is rare for a woman who
has an undetectable blood plasma viral load to have detectable HIV in vaginal
secretions.
A 2001 article in The
Lancet1 looked at 271 HIV-positive
women in the US Women’s Interagency HIV Study (WIHS) cohort study.
Three-quarters of the women were on HAART and half of them on PI-based
regimens. Both blood plasma and lymphocyte RNA measurements were performed on
the majority. Detectable viral RNA was found in the vaginal secretions of 130
out of 163 women (80%) with a blood plasma viral load of over 500 copies/ml,
and in 27 out of 83 women (33%) with a blood plasma viral load under that
figure. However, the researchers concluded that only one in ten of all the
women with detectable viral RNA in vaginal secretions had infectious virus.
A study in Italy2 divided 122 women into four
categories according to their experience of antiretroviral therapy: 55 women
were naive to therapy; 21 women were taking a break from antiretroviral
treatment due to treatment failure; 19 women were on treatment with one or two
NRTIs alone; and 28 were on highly active antiretroviral therapy (HAART).
This study found that almost three-quarters of the women on
non-HAART regimens had detectable plasma viral load (73%) and detectable (78%)
cervicovaginal viral load, 50% of women taking HAART had a detectable plasma
viral load, and 40% on HAART had detectable HIV in cervicovaginal secretions.
Looking only at the women who were on HAART or who were on
mono or dual therapy, 50% of women on HAART and 63% on mono or dual therapy had
undetectable viral loads (less than 80 copies/ml) in both blood and vaginal
secretions, and 29% of women on HAART and 11% on mono or dual therapy had
detectable viral loads in both. This left eleven women who were on some kind of
HIV therapy that had discordant viral loads. Twenty-one per cent of women on
HAART and 10% of women on mono or dual therapy had detectable HIV in their
blood, but none in their vaginal secretions: conversely 16% of women on mono or
dual therapy, but none on HAART, had detectable HIV in their vaginal secretions,
but none in their blood.
HAART was thus significantly associated with having a higher
viral load in blood than vaginal secretions, whereas suboptimal mono/dual
therapy was significantly associated with the opposite situation. The
explanation for this, and for low undetectability rates in general, was
probably that here was a group of women with quite advanced HIV disease (35%
had an AIDS diagnosis) and possible adherence issues (37% were injecting drug
users) who were taking therapy in the early days of HAART (1995-2001) before
the widespread use of boosted protease inhibitors.
Even in this situation, we note that no woman on HAART with
an undetectable viral load in blood had detectable virus in vaginal secretions.
This was not the case, however, in women on mono/dual therapy, or on no
therapy. In the latter case, amongst the 75 women taking no HIV drugs, one in
15 (6.7%) of women had no detectable viral load at all, one in twelve (8%) had
detectable HIV in blood but not in vaginal secretions, and just over one in 20
(5.3%) had detectable HIV in vaginal secretions but not in blood.
This has led researchers to tentatively conclude that while
it is probably rare for women with an
undetectable blood plasma viral load on HAART to have detectable vaginal HIV, the
same may not be the case for women who are undetectable off HAART.
Similarly, a later US longitudinal study in 97 women3 found that all of the
women with an undetectable viral load in the blood, and who were on HAART, also
had undetectable cervicovaginal viral loads. In women not on HAART, although
some did achieve undetectable plasma viral loads, some still had evidence of
cervicovaginal shedding: 5% of the time there were greater levels of virus in
the vagina than in the blood. When women achieved undetectable virus levels in
both the blood and vagina, rebound of virus occurred in the blood first or at
about the same time.
Successful antiretroviral therapy, however, cannot guarantee
that there will be no cervicovaginal shedding. A four-week study of 20 sex
workers in Mombasa, Kenya,4 found that seven women
(35%) continued to have detectable viral load in their genital secretions at
the end of the study. Similarly, although antiretroviral treatment
significantly reduced the frequency of genital shedding of HIV in a study
conducted in Burkina Faso,5 HIV remained detectable in
the genital tract of a significant proportion of women even when they had an
undetectable viral load in their blood. However, all the women in the study
were infected with the genital herpes virus HSV-2, and it is known that this can
increase genital shedding of HIV.
Other studies have found that viral load in the female
genital tract can vary during the course of a menstrual cycle, even among women
on antiretroviral treatment. A 2004 study6 of viral load changes
during the menstrual
cycle found that viral load levels in vaginal fluid tended to peak at the time
of menstruation and fell to the lowest level just prior to ovulation.