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Epstein-Barr virus (EBV) has been associated with primary central nervous system lymphoma and other EBV-related malignancies in HIV infected patients, and detection of EBV DNA in cerebrospinal fluid (CSF) by polymerase chain reaction (PCR) has been demonstrated to be a good marker of PCNSL. Conversely, EBV has been rarely associated with encephalitis in HIV patients. Here we describe for the first time the case of an HIV-infected, late presenter Caucasian man, diagnosed with a rapidly progressive diffuse encephalitis at presentation. A very high viral load for EBV was detected in CSF by PCR. The patient died 12 days after the onset of encephalitis in spite of supportive, antiviral and antiretroviral therapy. Our experience would suggest that in profoundly immunosuppressed HIV patients EBV may cause severe encephalitis in the absence of lymphoproliferative disorders.

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Coinfection by the Human Immunodeficiency Virus (HIV) and hepatitis viruses is a frequent condition in drug addicts. In the present study we report on the case of a patient with a history of drug and alcohol abuse who was sequentially infected with HIV, HCV, HBV and HDV. He died of an overwhelming reactivation of HBV and HDV in spite of a recent interferon treatment. HBV and HDV resumed their active replication after over 20 years of complete latency, that is after long-lasting viral undetectability, when the patient deliberately discontinued his last HAART regimen. HBV and HDV reactivated in spite of a relatively preserved immune system and a recent immune stimulatory treatment with pegylated interferon.

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Transmission of drug-resistant HIV-1 variants has been increasingly documented. The most commonly observed resistance-associated mutations are thymidine analogue mutations as well as non-nucleoside reverse transcriptase inhibitor mutations. We report on a case of secondary transmission of a protease inhibitor (PI) primary mutation from an infected untreated subject to his sexual partner. Sequences isolated from the 2 patients showed a high level of identity (>99%), both carrying the major IAS PI mutation M46I. The latter mutation persisted in the bloodstream of the female partner 1 year after its first detection.

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INTRODUCTION: Selection of the K103N mutation is associated with moderately reduced in vitro fitness of HIV. Strains bearing K103N in vivo tend to persist, even in the absence of additional drug pressure, as minority quasispecies, often undetectable in genotyping resistance testing assays, performed at standard conditions. Here, we report on the rapid and long lasting selection of a K103N bearing strain as the dominant quasispecies after very short exposure to efavirenz in vivo. CASE PRESENTATION: A 55-year-old Caucasian man was switched to efavirenz, zidovudine and lamivudine in February 2003, while on viral suppression in his first-line highly active anti-retroviral treatment regimen. One month later, he reported inconsistent adherence and his viremia level was 5700 c/mL. He did not attend further checkups until September 2005, when his viral load was 181,000 c/mL. The patient reported interrupting his medications approximately three weeks after simplification. The genotyping resistance testing assay was performed both on HIV RNA and HIV DNA from plasma, yielding an identical pattern with the isolate presence of the K103N mutation in the prevalent strain. CONCLUSION: Persistence of the K103N mutation as a majority quasispecies may ensue after a very short exposure to efavirenz. Our case would therefore suggest that the presence of the K103N mutation should always be ruled out by genotyping resistance testing assays, even after minimal exposures to efavirenz.

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The clinical spectrum of mixed cryoglobulinemia embraces several manifestations: recurrent vascular purpura, weakness, arthralgia/arthritis, glomerulonephritis, peripheral neuropathies, and Raynaud's phenomenon. Mixed cryoglobulinemia is currently treated with steroids, low-antigen content diet, immunosuppressors, plasma exchange, and antiviral therapy, namely, alpha -interferon alone or, more recently, in association with ribavirin. In the present research, we verified the effectiveness of combined therapy with interferon and ribavirin on asymptomatic mixed cryoglobulinemia in naïve (never treated before) patients with chronic hepatitis C. We enrolled 50 consecutive patients, 31 males and 19 females, with chronic hepatitis C who showed a sustained response to combined antiviral therapy (interferon and ribavirin). Before treatment, cryoglobulins were detected in 25 subjects (50%). Only 1 of the 25 patients with asymptomatic mixed cryoglobulinemia had persistence of cryoglobulins at the end of the follow-up period. Unexpectedly, in 7 of 25 subjects without mixed cryoglobulinemia before treatment, cryoglobulins became detectable after antiviral therapy. Our present study first reports the onset of asymptomatic mixed cryoglobulinemia in hepatitis C virus patients after clearance of the virus from blood obtained with a combined antiviral treatment. Possible explanations are discussed. Our data also suggest that the appearance of a clinically evident mixed cryoglobulinemia cannot be excluded in this kind of subject.

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