Biomedical subjects

A R Buonomini

Publications and source records attributed to A R Buonomini.

3 recordsLinked to original sources

PubMed2007

Human herpesvirus 8 and human herpesvirus 2 infections in prison population.

Incarcerated persons have high rates of infectious diseases. Few data on the prevalence of sexually transmitted diseases in prisoners are available. This multi-center cross-sectional study enrolled 973 inmates from eight Italian prisons. Demographic and behavioral data were collected using an anonymous standardized questionnaire and antibodies to HIV, HCV, HBV, HSV-2, and HHV-8 were detected in a blood sample obtained from each person at the time of the enrollment in the study. Two hundred and two out of the 973 subjects (20.7%) had antibodies against HHV-8. HHV-8-seropositive subjects were more likely to be older than 30 years with a higher educational level. HHV-8 infection was associated significantly with HBV (P < 0.001) and HSV-2 (P = 0.004) seropositivity and with previous imprisonments. Multivariate analysis showed that HHV-8 infection in Italian inmates was associated with HBV (P < 0.001) and HSV-2 (P = 0.002) seropositivity otherwise among foreigners inmates HHV-8 was significantly associated with HBV infection (P = 0.05). One hundred and eighty-six (21.2%) prisoners had anti-HSV-2 antibodies. At multivariate analysis HSV-2-positivity was significantly associated with HIV (P < 0.001) and HHV-8 infections (P = 0.003), whereas it was inversely associated with HCV infection (0.004). A relatively high seroprevalence of HHV-8 and HSV-2 among Italian prison inmates was found. The association of HHV-8 and HSV-2 infections suggest sexual transmission of these viruses among Italian prison inmates.

Adult↗

PubMed2004

Decrease of replicative capacity of HIV isolates after genotypic guided change of therapy.

A longitudinal study of the replication capacity of HIV strains isolated from 18 patients failing highly active antiretroviral therapy (HAART) was undertaken at the time of genotypic guided change of therapy and after 12 months. Patients were divided in two groups according to the response to therapy: immune responders (12 patients with immune recovery defined as having more than 100 CD4 cells compared to baseline value), and failing patients (six patients without immune recovery). At enrollment no significant difference in terms of CD4 cell count and HIV plasma viremia was detected between the two groups. One year after change of therapy, all patients experienced a decrease in the replication capacity of HIV strains. The HIV replication capacity of the failing and of immune-responder patients decreased from 60% (range 14-96%) to 26.4% (range 0.4-74.5) and from 46.8% (range 15-98%) to 3.6% (range 0.1-26.8%), respectively. At month 12, the difference of HIV replication capacity between the two groups reached a statistical significance (P<0.03). After the change of therapy, an increase in the number of drug resistance mutations in the protease gene was detected in both groups with a higher prevalence of M36I mutation in immune responders. The HIV strains of patients failing HAART showed a progressive impaired replication capacity. The degree of the impairment in viral replication correlated with the viro-immunological discordant response to HAART and with the acquisition of new drug resistant mutations in the protease gene. In patients failing HAART, the impaired replication capacity of HIV strains could justify the persistence of an immune recovery.

Adult↗

PubMed2004

Discordant response to HAART: reduction of viremia and replicative capacity of HIV strains in patients after genotype guided change of therapy.

The aim of this study was to evaluate outcome after a genotype guided change of therapy in 18 patients failing HAART. Patients were divided into two groups according to the response to therapy: immune responders (12 patients with immune recovery defined as having more than 100 CD4 cells compared to baseline value), and 6 failing patients (without immune recovery). At month 12 after genotype change of therapy a significant difference in the decrease of HIV-RNA viral load between the two groups of patients was detected (mean -1.95 and +0.04 log HIV-RNA copies/ml, p=0.04). One year after the change of therapy, all but one patients experienced a decrease in the replication capacity of HIV strains. Particularly, the HIV replication capacity of HIV strains decreased from 52% (range 14-98%) to 15.2% (range 0.1-74.5%). The HIV strains of patients failing HAART showed a progressive impaired replication capacity. In patients failing HAART the impaired replication capacity of HIV strains could justify the persistence of an immune recovery.

Adult↗