Early syphilis infection lowers CD4 count and raises viral load in HIV-positive patients

A third study has found that syphilis infection in HIV-positive patients is associated with increases in viral load and decreases in CD4 cell count. The Spanish study, published in the March 1^st issue of the Journal of Acquired Immune Deficiency Syndromes, is the largest of the three and, its authors believe, the first to have analysed the factors associated with changes in viral load and CD4 cell count during syphilis infection.

The investigators found that syphilis infection was associated with CD4 count decreases and viral load increases in almost one third of the patients studied. Their results showed that the only factor associated with an increase in HIV viral load was not being on antiretroviral therapy (ART), while the only factor associated with a fall in CD4 cell count of more than 100 cells/mm³ was the patient’s pre-syphilis CD4 cell count (patients who had higher pre-syphilis CD4 counts experienced greater falls).

The study’s authors highlight one other finding from their study: more than two thirds of the syphilis cases were diagnosed in patients who had previously been diagnosed HIV-positive. This, they say, “highlights the risky behaviour of our patients” and their “weak preventive strategies”. They call for public health efforts to prevent new syphilis infections and to identify and treat infected patients as soon as possible, in order to reduce the spread of both syphilis and HIV.

The study was a retrospective one, using data from twelve Spanish hospitals. Researchers identified all the HIV-positive patients who had been diagnosed with early (less than two years) syphilis infection between January 2004 and December 2005. Patients who began or changed HIV treatments during the analysis period were excluded.

One hundred and eighteen patients were analysed. Of these, 95.8% were men, 83.9% were gay, 50.8% were on ART at the time their syphilis was diagnosed, and 32.2 % had received their HIV and syphilis diagnoses at the same time. Mean patient age was 38.2 years.

The investigators compared the patients’ plasma viral load measurements and CD4 cell counts at three points during the analysis period: 3-9 months before the diagnosis of syphilis, during the infection (between twelve and two weeks before the syphilis diagnosis), and three to nine months after diagnosis and treatment. For all the patients, treatment consisted of standard doses of benzathine penicillin.

Viral load and CD4 cell measurements “before” and “during” syphilis were available for 76 participants. Thirty-two of these had detectable viral loads before their syphilis diagnosis, ten (33.3%) of whom demonstrated viral load increases during the infection. The other forty-four patients had a fully suppressed viral load before their syphilis diagnosis, and eleven (25%) of them demonstrated a detectable viral load during their infection. Even so, the only factor associated with an increase in viral load was not being on ART.

The 76 patients with “before-to-during” data also showed significant decreases in CD4 cell counts during syphilis infection (590 vs. 496 cells/mm³; P = 0.0001), and the 94 who had “during-to-after” data showed significant increases in CD4 count after their syphilis was treated (509 vs. 597 cells/mm³; P = 0.0001).

The authors note that though it has previously been thought that increases in viral load occur mainly among patients with secondary syphilis infection, “our study [found] no difference in the virologic change depending on the stage of the syphilis”. They also note that, in line with several other studies of coinfection in HIV-positive patients, they found no reduction in viral load after the syphilis was treated. These findings are thought to be the result of persisting immune activation.