Prevalence of human papillomavirus infection,distribution of viral types and risk factors in cervical samples from human immunodeficiency virus-positive women attending three human immunodeficiency virus-acquired immune deficiency syndrome reference centres in northeastern Brazil

Human immunodeficiency virus (HIV)-positive patients have a greater prevalence of coinfection with human papillomavirus (HPV) is of high oncogenic risk. Indeed, the presence of the virus favours intraepithelial squamous cell lesion progression and may induce cancer. The aim of this study was to evaluate the prevalence of HPV infection, distribution of HPV types and risk factors among HIV-positive patients. Cervical samples from 450 HIV-positive patients were analysed with regard to oncotic cytology, colposcopy and HPV presence and type by means of polymerase chain reaction and sequencing. The results were analysed by comparing demographic data and data relating to HPV and HIV infection. The prevalence of HPV was 47.5%. Among the HPV-positive samples, 59% included viral types of high oncogenic risk. Multivariate analysis showed an association between HPV infection and the presence of cytological alterations (p = 0.003), age greater than or equal to 35 years (p = 0.002), number of partners greater than three (p = 0.002), CD4⁺ lymphocyte count < 200/mm³ (p = 0.041) and alcohol abuse (p = 0.004). Although high-risk HPV was present in the majority of the lesions studied, the low frequency of HPV 16 (3.3%), low occurrence of cervical lesions and preserved immunological state in most of the HIV-positive patients were factors that may explain the low occurrence of precancerous cervical lesions in this population.     

Kinetics of uranous iron and ferrous iron oxidation by thiobacillus ferrooxidans

Archives of Microbiology -     

Cloning and expression of the 3C-proteinase gene from the poliomyelitis virus in E. coli cells]

Expression of the 3C protease gene of poliovirus type 1 (Mahoney) in E. coli cells using various vectors was studied. The 3C gene was shown to be expressed effectively upon its cloning in HindII/HindII (bases 5240 to 6770) and in HindII/HindIII (bases 5240 to 6056) fragments of poliovirus cDNA in pTTQ8 vector containing tac-promoter and lacI-repressor gene. Products of processing at the N-terminal 3C protease Gln-Gly site and polypeptides formed upon translation from an alternative methionine, which was coded by bases 5516-5518 of poliovirus cDNA, were found among virus-specific proteins. Processing at the C-terminal 3C protease Gln-Gly site was not observed.     

Uncharged P-selectin blockers

The blocking potency of P- and L-selectin was studied for certain small molecule mannosides and their polyacrylamide (PAA, 30 kDa) conjugates in comparison to SiaLe^x and fucoidan. Two experimental systems were used: (1) solid phase static assay based on recombinant selectins, and (2) P-selectin dependent rat peritoneal inflammation. βMan-SC₆H₄NO₂-p was four times more potent P-selectin inhibitor as compared to SiaLe^x. Docking of this molecule onto the P-selectin carbohydrate-binding site demonstrated that a nitro group enabled an electrostatic interaction with residue Lys 84, while the phenyl ring and the CH₂ at C-6 contacted the CH₂ groups of the same Lys residue. In vivo, βMan-SC₆H₄NO₂-p blocked experimental inflammation better than SiaLe^x, but significantly lower than fucoidan. In vitro Man-polyacrylic acid conjugates appeared to be very potent inhibitors comparable to fucoidan, uncharged Man-PAA proved rather active, comparable to SiaLe^x-PAA both in vitro, and in vivo, whereas mannan did not display any P-selectin blocking effect. Published in 2004. This revised version was published online in July 2006 with corrections to the Cover Date.     

Role of nucleases in the origination of chromosomal disorders in virus-infected cells]

It is shown that herpes simplex virus can induce the chromosome aberrations both in cells supporting the productive infection and in non-permissive cells. In virus-infected human embryo fibroblast culture the activity of cell (lysosomal) and virus-coded DNAses is elevated. Suppression of the activity of any of the enzymes leads to decreasing the number of aberrant cells. Suppression of the activity of both DNases at the same time decreases the number of aberrant cells to a control level. In M15 cells which do not support the productive infection, the activity of only lysosomal DNase is elevated. Suppression of its activity leads to the decrease of the frequency of cells with chromosome breaks to a control level. Thus, both cells and virus-coded lytic enzymes can participate in the production of chromosome breaks in virus-infected cells. Possibly, the relative role of these enzymes may be rather different in different virus-cell systems.