Within the limits of the relatively small sample size, Peg-IFNalpha-2a and Peg-IFNalpha-2b demonstrated nonstatistically significant differences in effectiveness in patients nonresponsive to previous antiviral treatment.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 The influence of antiretroviral therapy on co-receptor tropism remains controversial. To 25 verify if co-receptor tropism shift was affected by HAART, the evolution of proviral DNA V3 26 genotype after 12 months of a new antiretroviral regimen was compared between 27 responder and non-responder patients. 28Baseline blood samples were collected from 36 patients infected with HIV-1 subtype-B (18 29 naïve and 18 experienced) for virus isolation and env V3 genotyping from plasma HIV-1 30 RNA and PBMC DNA. DNA V3 genotyping was repeated after 12 months from initiating 31 HAART. WebPSSM was used for categorizing V3 sequences into X4 or R5; for analysis 32 purposes, dual/mixed viruses were considered as X4. 33From the 10 (28%) patients changing their proviral DNA V3 genotype during therapy, six 34shifted from R5-to-X4 and four from X4-to-R5. The lack of reaching virological suppression 35 was not associated with an X4-to-R5 (p=0.25) or R5-to-X4 (p=0.14) shift; time-to-viral 36 suppression and CD4 increase were similar in both groups. No association was found 37 between tropism shift and patient baseline characteristics including age, sex, CDC stage, 38 CD4 count, viral load, exposure and length of previous HAART, enfuvirtide use in the new 39 regimen, number of reverse-transcriptase and protease resistance-associated mutations. 40Conversely, CD4 nadir was correlated to emergence of X4 virus in proviral DNA (mean 41 27.2±30.6 in R5-to-X4 shifting patients vs 161.6±150.6 in non-shifting patients, p=0.02). 42The occurrence of a tropism shift in both directions was independent of HAART use, 43 irrespective of its efficacy. The CD4 count nadir was the only baseline characteristic able 44 to predict an R5-to-X4 viral shift. 45

An extended spectrum of HIV-1 reverse-transcriptase (RT) mutations in HAART-treated patients has been recently described. To verify the possible association of previously unreported RT mutations with a decrease of phenotypic susceptibility to nucleoside (NRTIs) and non-nucleoside (NNRTIs) RT inhibitors, the RT sequence of 328 HIV-1-positive patients (102 naïve and 226 treated with HAART participating in either the PhenGen or Genpherex study) was analyzed. All treated patients were tested at the time of therapeutic failure with both phenotypic (Antivirogram 1 , Virco) and genotypic analyses (VircoGen TM ); the frequency of RT substitutions (positions 1-240) with respect to consensus B was compared to that of naïve patients using a Chi-square test. Amino acid changes at 13 positions not included in the IAS list of resistance-associated mutations were detected more frequently in treated than in naïve subjects. The mutations involving 10 of these positions were associated with a reduced susceptibility to antiretroviral drugs; K20R, T39A, K43EQN, E203KD, H208Y, and D218E were correlated with NRTI resistance while mutations K101EQP, H221Y, K223EQ, L228HR were associated to NNRTI resistance. A correlation was found between K20R and lamivudine resistance (P ¼ 0.006) while T39A (P ¼ 0.005), K43EQN (<0.001), E203KD (P ¼ 0.010), and H208Y (P ¼ < 0.001) seemed to be associated with a previous use of zidovudine and stavudine and with the development of thymidine analog resistance. For H208Y, an association with use/resistance to abacavir (P ¼ 0.004) was also noted. D218E showed a weak association to didanosine resistance (P ¼ 0.013). The data confirm that previously unreported mutations are associated with antiretroviral drug experience and, more importantly, with a reduced susceptibility to NRTIs and NNRTIs.

In this study we assessed the seroprevalence of hepatitis E virus (HEV) infection in both the Italian population and immigrants from developing countries in Foggia (Apulia, Southern Italy). The seroprevalence of HEV was determined in 1217 subjects [412 (34%) immigrants and 805 Italian subjects (blood donors, general population, HIV-positive, haemodialysis patients)]. Serum samples were tested for anti-HEV and confirmed by Western blot assay; in positive patients HEV RNA and genotype were also determined. There were 8·8% of patients that were positive to anti-HEV, confirmed by Western blot. The prevalence in immigrants was 19·7%, and in Italians 3·9% (blood donors 1·3%, general population 2·7%, HIV-positive patients 2·0%, haemodialysis patients 9·6%). Anti-HEV IgM was found in 38/107 (35·5%) of the anti-HEV-positive serum samples (34 immigrants, four Italians). This study indicates a higher circulation of HEV in immigrants and Italian haemodialysis patients, whereas a low prevalence of HEV antibodies was seen in the remaining Italian population.

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