|The Eternal Quest (HERPES AND HIV, 2010)
Dec 19, 2010
Dear Dr. Bob,
May I be the first (along with my kitty here draped over my arm while I type) to wish you a "Merry Christmas". Just don't snog to much on the eggnog, OK? :)
Well, I pulled out my trusty "BS meter" and wanted to verify if yours was on the same wavelength concerning "Humic Acid" which I'm reading right now is a "breakthrough discovery" with the "missing link" in our food chain that can "regulate the immune system cells and prevents either T or Killer cells from becoming out of balance".
Of course, the humic acid or humate, is vaguely tied to squashing HIV and a host of other ills in your check-off box which you need to fill out before you can get the pills that they're pushing.
Sigh. I just couldn't find the box where swallowing those pills could reduce the size of my thunder thighs. Now, THAT would be a true medical breakthrough.
All silliness aside, what is your take on this? I checked the archives and there's a comment from 2008 stating some test tube studies with HIV but nothing else of clinical significance. Any noteworthy updates?
And, staying in the H_V category, is there any progress on HSV 1 and 2? Since HIV is greatly enhanced on transmission if a person has HSV 2, why isn't there good, forward research on this virus that affects millions? If HSV could be reduced/wiped-out/controlled then HIV transmission could be slowed if even a small amount. It seems acyclovir and it's variants are the only medicines out there and has been for many years.
Also, thank you in advance for reading this e-mail. Your tireless efforts have really helped so many people.
Response from Dr. Frascino
Thanks for the Happy Festivus greeting.
Your bullshit meter remains finely calibrated. Humic Acid is indeed another SCAM. I'm confident thunder thigh reduction will be listed on subsequent boxes of this worthless product.
Regarding HSV, there has actually been quite a bit of research. I'll reprint the latest findings below.
Finally, Happy Thankschristkwanzaakkah!
Herpes Simplex Virus Type 2 Infection Twenty years' worth of epidemiologic data support a synergistic relationship between herpes simplex virus type 2 (HSV-2) and HIV infections. Reactivation of HSV-2 increases HIV susceptibility and infectiousness and potentially accelerates HIV disease progression. Also, HIV infection increases the frequency of HSV-2 outbreaks, facilitating HSV-2 transmission. Numerous longitudinal studies that were adjusted for age and sexual behavior have shown that prevalent HSV-2 infection is associated with a statistically significant increase in the relative risk (RR) of HIV acquisition in men (RR, 2.7), women (RR, 3.1), and men who have sex with men (MSM; RR, 1.7). The risk of HIV acquisition appears to be even higher in patients with incident (recently acquired) HSV-2 infection (RR, ~ 6), although it is difficult to discern whether individuals acquired HSV-2 infection before or at the same time as HIV infection. In some African locales where HSV-2 prevalence is very high, mathematical modeling and epidemiologic analyses estimate that up to one-third to one-half of new HIV infections can be attributed to HSV-2 infection. Biological plausibility for increased HIV susceptibility comes from various lines of evidence. These include studies showing that HSV-2 causes macroscopic and microscopic ulcerations and that HSV-2 reactivation is quite frequent. Studies of HIV-seronegative persons in which patient-obtained genital swabs were tested by HSV polymerase chain reaction show that reactivation occurs on 20% of days and even more frequently if HSV shedding is evaluated more than once daily (Mark et al, J Infect Dis , 2008). Also, HSV-2-infected women who were not necessarily shedding virus had increased populations of HIV target cells, specifically immature dendritic cells and cervical CD4+ T cells expressing CC chemokine receptor 5 (CCR5) (Rebbapragada et al, AIDS , 2007). Such data provided the rationale for investigating whether suppression of HSV-2 could reduce acquisition of HIV. In a placebo-controlled study in 821 HSV-2-seropositive, HIV-seronegative Tanzanian women at high risk of HIV infectiona study in which the drop-out rate was high, adherence was modest, and clinic visits occurred only quarterlytwice-daily acyclovir 400 mg showed no effect in preventing HIV acquisition (Watson-Jones et al, N Engl J Med , 2008). Another trial conducted with the same acyclovir dose in more than 3000 HSV-2- seropositive, HIV-seronegative women in African locales and MSM in Peru and the United States also showed no preventive effect in HIV acquisition (Celum et al, Lancet , 2008). A potential explanation for why HSV-2 suppression did not reduce risk of HIV acquisition is provided by recent data supporting a "sparks-andembers" model of continued susceptibility even in patients with suppressed HSV-2 outbreaks. These data show that as the host genital mucosal immune system persistently encounters HSV-2 antigen, localized persistence of CCR5+ cells is imprinted in genital skin and mucosa, resulting in a 10-fold increase in CD4+ cells and dendritic cells in the genital epithelium that lasts for more than 8 weeks after HSV-2 reactivation (Zhu et al, Nat Med , 2009). The increased infiltration of HIV target cells ("sparks") and increased local enhancement ("embers") provides HIV with an advantage in an initial contact between HIV and host. Although current HSV-2 drugs can suppress reactivation, they do not reduce the persistent inflammation of the genital mucosal HIV target cells. Thus, the susceptibility to HIV acquisition remains increased. Other studies have evaluated whether suppression of HSV-2 in patients coinfected with HIV can reduce HIV infectiousness or HIV disease progression. The plausibility of such effects is supported by a number of findings. First, data from the prepotent antiretroviral therapy era indicated that the addition of high-dose acyclovir to nucleoside analogue reverse transcriptase inhibitor (nRTI) treatment improved survival. Second, HSV-2 reactivation is more frequent in HIVinfected persons than in uninfected persons. Lesions persist longer and high amounts of HIV RNA are present in lesion fluid (exceeding plasma levels). Third, increased levels of plasma and genital HIV RNA are present during even asymptomatic HSV-2 reactivation. Fourth, HSV proteins produced during reactivation have been demonstrated to upregulate HIV replication in vitro. Finally, numerous studies (generally small and with short follow-up periods) have shown that in HIV-infected persons with CD4+ cell counts greater than 250/μL who are not receiving antiretroviral therapy, acyclovir or valacyclovir suppressive therapy is associated with reductions in HIV RNA levels in plasma (by 0.3 log10 −0.5 log10 copies/ mL) and in rectal, seminal, and cervical secretions. In the recent Partners in Prevention HIV and HSV transmission study conducted in 7 countries in Africa, each HIV- and HSV-2-coinfected person in 3400 HIV-serodiscordant couples was randomly assigned to receive twicedaily acyclovir 400 mg or placebo, and the couples were observed for up to 2 years (Celum et al, N Engl J Med , 2010; Lingappa et al, Lancet , 2010). The HIV-infected partners had CD4+ cell counts of 250/μL or greater (the national guidelines threshold for initiating antiretroviral therapy) and were not receiving antiretroviral therapy at study entry. Over the 2 years, acyclovir treatment was not associated with a statistically significant prevention of HIV acquisition (hazard ratio, 0.92; 95% confidence interval, 0.60−1.41; P =.69), despite a 0.25 log10 copies/mL reduction in plasma HIV RNA level and a 0.75 log10 copies/mL reduction in genital ulcer secretions. However, acyclovir suppression was associated with a statistically significant 16% reduction in HIV disease progression measured as the composite of decrease in CD4+ cell count to less than 250/μL, initiation of antiretroviral treatment, or death. Treatment was also associated with a statistically significant 19% reduction in progression to CD4+ cell counts of less than 350/μL in patients entering the study with counts above this level. The lessons learned from the recent intervention studies include the following: a suppressive regimen (twice-daily acyclovir 400 mg) does not resolve persistent inflammation caused by HSV infection; such suppressive treatment does not prevent HIV transmission despite reductions in HSV-2 outbreaks and a 0.25 log10 copies/mL reduction in plasma HIV RNA levels; and twicedaily acyclovir 400 mg modestly reduces progression of HIV disease in patients not receiving antiretroviral therapy who have CD4+ cell counts of 250/μL or greater. One conclusion is that for patients coinfected with HIV and HSV-2, practitioners could consider initiating antiretroviral therapy earlier for those with CD4+ cell counts greater than 350/μL to reduce their likelihood of HIV transmission and for clinical benefits. Another conclusion is that further consideration should be made of the potential use of HSV-2 suppressive treatment in coinfected patients with CD4+ cell counts greater than 350/μL who are not eligible for or who elect not to initiate antiretroviral therapy. A third conclusion is that more effective drugs for HSV-2 infection are needed, as is a genital herpes vaccine. Unfortunately, the recently released results of the Herpevac Trial for Women (cosponsored by the National Institute of Allergy and Infectious Diseases and GlaxoSmithKline) of a candidate HSV-2 vaccine in HSV-1- and HSV-2-seronegative women showed no efficacy, and the pipeline for other HSV-2 vaccine candidates is limited. The interaction of HSV-2 and HIV infections emphasizes the importance of genital herpes testing and appropriate counseling. Type-specific HSV-2 serology tests may be useful for patients with recurrent and atypical symptoms and negative culture results, for patients with a clinical diagnosis of HSV-2 but no laboratory confirmation, and for patients with a sexual partner with genital HSV infection. Type-specific testing might also be appropriate for patients presenting for comprehensive STI evaluation, for those with HIV infection or several sexual partners, and for MSM with high risk of acquiring HIV. Type-specific enzyme immunoassays (EIAs) for HSV-2 have sensitivity and specificity of 97%, and results can be expected to become positive within 3 weeks after the acquisition of HSV-2 infection. Updated STI guidelines are expected soon from the US Centers for Disease Control and Prevention (CDC) regarding recommendations for serologic testing for HIV-infected patients and for those with high-risk behaviors for HIV acquisition.
Please Help me.
How long does it take?
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