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Preventing hepatitis B by vaccination is essential in HIV-infected patients (higher progression rate of HBV infection to chronicity, lower rate of serum HBe Ag loss). However, it has been shown a decreased anti-HBs response in these individuals after a standard vaccination (3 doses of 20 micrograms). Thus, we tested the hypothesis that doubling the number of hepatitis B vaccine injections might increase anti-HBs response rate. HIV-infected patients with CD4 > 200/microliter, who were on stable antiretroviral treatment, as well as seronegative for HBV markers, and who have never been vaccinated against HBV, were given 3 intramuscular injections of Genhevac B 20 micrograms at 1 month intervals. Initial non responders were given 3 additional monthly injections. Anti-HBs titer was followed. We also evaluated the effects on HIV-1 viral load. Twenty patients with a median CD4 cell count of 470/microliter were enrolled. The response rate after three 20 micrograms injections was 55% (11/20), lower in individuals with CD4 between 200 and 500/microliter (4/12 = 33.3%), compared to patients with CD4 above 500/microliter (7/8 = 87.5%, P = 0.02). Among 9 initial non-responders, only 2 did not respond to 3 additional doses; thus, the overall response rate was 90% (18/20). Geometric mean titers of anti-HBs were 133 IU/l and 77.5 IU/l, after 3 and 6 Genhevac doses, respectively (P = 0.38). One year later, only 10/17 (58.8%) patients had protective anti-HBs. Five patients experienced a significant viral load increase, transient in 3 cases. These preliminary results suggest that doubling the number of hepatitis B vaccinations in HIV-infected patients might significantly improve anti-HBs response rate; however, close monitoring of anti-HBs is necessary because of its short-lived persistence. The effects on HIV-1 viral load are limited.

Objective: Many cases of porphyria cutanea tarda have been described in association with human immunodeficiency virus (HIV) infection in young individuals. The link between hepatitis C virus (HCV) and porphyria cutanea tarda is even stronger as more than 50% of patients who have this diagnosis in Italy, France, or Spain are also infected by HCV. To study the role of viral infections on the metabolism of porphyrins, we measured the urinary porphyrin levels in patients with HIV and HCV infections., Design: Survey; prospective study., Setting: University Hospital of Strasbourg, France., Patients: Sixty-one HIV-positive patients, 56 HCV-positive patients, 60 HIV- and HCV-positive patients, and 51 HIV- and HCV-negative control subjects were randomly selected. None had clinical signs of porphyria or a familial history of porphyria., Main Outcome Measures: The porphyrin-excretion profile was determined by high-performance liquid chromatography on fresh urine samples. The HIV and HCV viremias were quantified in the serum by the branched DNA assay. Measures were planned before data collection began., Results: The porphyrin-excretion profile typical of porphyria cutanea tarda was found in only 1 of 177 patients. In the remaining 176 patients, the mean coproporphyrin level was significantly raised in HCV-positive patients and even higher in patients who were HIV- and HCV-positive. The coproporphyrin level was not correlated to the alanine aminotransferase level, the CD4+ cell count, or the HCV and HIV viremias., Conclusions: In cases of infection with HIV, HCV, or both, the development of a porphyria cutanea tarda urinary profile is a rare event (0.56% in this study), but coproporphyrin excretion is increased. This could be related to hepatic changes induced by the viruses. Our results do not support the hypothesis of a direct viral effect on the porphyrin metabolism. Infection with HIV, HCV, or both may be a major triggering factor, but is not sufficient to induce porphyria.

In patients chronically infected by hepatitis C virus (HCV), peripheral blood mononuclear cells (PBMCs) were shown to be targets for virus replication and in those coinfected with HIV, HCV viraemia was considerably increased. The purpose of this study was to quantify HCV RNA in PBMCs from 25 patients infected by HCV and from 25 patients coinfected by HCV and HIV. We used the branched DNA assay after extraction of total RNA on 5 x 10(6) cells to quantify HCV RNA, and the Inno LiPA assay to determine the HCV genotype. HCV RNA in PBMCs could be quantified in 8/25 patients in each group, but the HCV RNA concentration was very low in comparison with viraemia, since the highest result was 8.1 x 10(4) Eq genome/10(6) cells. In 10 ml of total blood, there was approximately 100 to 5,000 times less HCV RNA in PBMCs than in the plasma. It is therefore likely that PBMCs play only a minor part in the viral load present in the plasma. There was no preferential genotype associated with quantifiable HCV RNA in the PBMCs. In the case of HIV coinfection, there was no increase in the HCV-RNA concentration in PBMCs that could explain the increased viraemia observed in these patients. On the contrary, HCV RNA could not even be detected by RT-PCR in some of our coinfected patients.