Objective A prospective study was carried out to assess HIV‐1 and HIV‐2 mother‐to‐child transmission (MTCT) rates in Portugal between 1999 and 2005 by analysing the proportion of diagnosed infected children born to HIV‐positive mothers. Materials and methods Serial blood samples were collected from 1315 children at risk of HIV‐1 infection, 131 children at risk of HIV‐2 infection and six children at risk of both HIV‐1 and HIV‐2 infections attending 25 Health Institutions. HIV proviral DNA was detected by nested polymerase chain reaction (PCR) and statistical analysis was performed using spss. Results DNA PCR using HIV‐1 and HIV‐2 long terminal repeat (LTR) primers amplified 92.5% and 75% of maternal HIV infections, respectively. Overall, MTCT occurred in 3.4% [95% confidence interval (CI) 2.5–4.6%] of HIV‐1 and 1.5% (95% CI 0.2–5.4%) of HIV‐2 mother–child pairs. A significant decrease in HIV‐1 MTCT was observed with time, from 7.0% (95% CI 2.6–14.6%) in 1999 to 0.5% (95% CI 0.0–2.5%) in 2005. HIV MTCT was associated with an absence of antiretroviral therapy in infected pregnant women (P<0.0001). Of the 48 infected children (46 with HIV‐1 and two with HIV‐2), the schedule of blood sample collection was followed for only 26 children. In 14 (53.8%) of those 26 children the infections were diagnosed in the first sample collected before they were 48 h old, suggesting in utero transmission. Despite the national recommendations for antenatal HIV testing, a high overall proportion (22.2% for HIV‐1 and 44.3% for HIV‐2) of mothers did not access any MTCT prevention measures, mostly because of late diagnosis in pregnancy. A small but significant proportion of HIV‐2 infection was found in mothers with no identifiable link with West Africa. Conclusion HIV‐2 transmission rates are low (1.5% in this study), and this may have led to a lower uptake of interventions, but in the absence of interventions transmission does occur. HIV‐1 transmission was also associated with a lack of intervention, mostly as a result of late presentation. Use of primers restricted to a single sequence led to false‐negative maternal results in a significant proportion of cases. In part this may have been attributable to very low HIV DNA loads as well as primer template mismatches. HIV infection was not documented in children born to mothers with negative HIV DNA PCR results.

Over the past decade, Portugal and Spain received large numbers of immigrants from HTLV-1 endemic areas. Our aim was to investigate the diversity of subtypes circulating in these two countries and the introduction of new variants. We performed a molecular analysis of HTLV-1 strains in patients diagnosed since 1998. LTR and env proviral sequences from 26 individuals were analyzed to generate phylogenetic trees along with reference HTLV-1 subtypes from several geographic origins. Epidemiological and clinical data were recorded. Most subjects were immigrants (57.7%) from South America and Africa. All isolates belonged to the cosmopolitan A subtype. Most carried the transcontinental subgroup A, but five subjects carried subgroup D and one carried subgroup C, previously unreported in Europe. HTLV strains showed separate clusters linked to the patients' geographic origin. Although subjects with HTLV-1 infection tend not to be engaged in high-risk practices, silent dissemination of a broad diversity of HTLV-1 viruses may still occur.

Until today, the susceptibility of human immunodeficiency virus type 2 (HIV-2) to protease and nucleosidic reverse-transcriptase inhibitors (PI and NRTI, respectively) has not been clearly documented. In this report we studied HIV-2 proviral sequences (n = 30) from drug-naive patients. Our results revealed that several amino acid positions in the protease and reverse transcriptase coding sequence harbored residues that have been associated with drug resistance in HIV-1-infected patients. In particular, the M46I substitution in the protease was detected in 90% of the sequences analyzed, which, together with the other substitutions identified, may indicate a reduced susceptibility of HIV-2-infected drug-naive patients to PI. Furthermore, interpretation of genotypic data with four available algorithms, developed for interpretation of HIV-1 sequence data, suggested nonoverlapping profiles of drug resistance.

Human immunodeficiency virus type 2 (HIV-2) infections cause severe immunodeficiency in humans, although HIV-2 is associated frequently with reduced virulence and pathogenicity compared to HIV-1. Genetic determinants that play a role in HIV pathogenesis are relatively poorly understood but nef has been implicated in inducing a more pathogenic phenotype in vivo. However, relatively little is known about the role of nef in HIV-2 pathogenesis. To address this, the genetic composition of 44 nef alleles from 37 HIV-2-infected individuals in Portugal, encompassing a wide spectrum of disease associations, CD4 counts and virus load, has been assessed. All nef alleles were subtype A, with no evidence of gross deletions, truncations or disruptions in the nef-encoding sequence; all were full-length and intact. HIV-2 long terminal repeat sequences were conserved and also indicated subtype A infections. Detailed analysis of motifs that mediate nef function in HIV-1 and simian immunodeficiency virus, such as CD4 downregulation and putative SH2/SH3 interactions, revealed significant natural variation. In particular, the central P104xxPLR motif exhibited wide interpatient variation, ranging from an HIV-1-like tetra-proline structure (PxxP)3 to a disrupted minimal core motif (P104xxQLR). The P107→Q substitution was associated with an asymptomatic phenotype (Fisher's exact test, P=0·026) and low virus loads. These data indicate that discrete differences in the nef gene sequence rather than gross structural changes are more likely to play a role in HIV-2 pathogenesis mediated via specific functional interactions.