Summary: For 4 years, we determined the mode and risk of mother-to-child transmission of HTLV-I in a prospective cohort of 34 children born to seropositive mothers in Franceville, Gabon. We also determined the prevalence of antibodies to HTLV-I/II in siblings born to seropositive mothers. Antibodies to HTLV-I/II were detected by Western blot, and the proviral DNA was detected by the polymerase chain reaction (PCR). The risk of seroconversion to anti-HTLV-I for the 4 years of follow-up was 17.5%. Anti-HTLV-I/II and proviral DNA were only detected after age 18 months. We observed a seroprevalence rate of 15% among the siblings born to HTLV-I/II seropositive mothers. Furthermore, we report a case of mother-to-child transmission of HTLV-II infection in a population of HTLV-II-infected pregnant women that is emerging in Gabon. The lack of detection of HTLV-I/II proviral DNA in cord blood and amniotic fluid and, furthermore, the late seroconversion observed in the children indirectly indicate that mother-to-child transmission occurred postnatally, probably through breast milk.
Summary: Twenty‐nine children with acute icteric hepatitis were classified as follows after serological tests for the agents of viral hepatitis: hepatitis B 17 patients, hepatitis A 3 patients, hepatitis A + B 1 patient, possible non‐A, non‐B hepatitis 8 patients. In four of these cases, hepatitis A or non‐A, non‐B occurred in chronic HBsAg carriers. Hepatitis B virus (HBV) DNA was present in the initial serum of 15 of the 18 patients with acute hepatitis B. About 1 year after onset, HBsAg and HBV DNA were absent in 17 of them (16 of whom developed anti‐HBs) and the remaining patient became a chronic HBsAg carrier without HBV DNA in his serum. At the same time, liver biopsy samples from all 29 patients were available for HBV DNA investigation. HBV DNA sequences in the liver were never found in any patient, neither under free form nor integrated into the cellular genome. The absence of HBV DNA integration in any of the liver samples taken about 1 year after the acute phase of hepatitis B suggests that such integration is either unlikely or is transitory during the symptomatic period.
Nef is an accessory protein critical for the ability of human and simian immunodeficiency viruses (HIV and SIV) to replicate efficiently in their respective hosts. Previous analyses of members of 15 different primate lentivirus lineages revealed a link between Nef function and the presence of a vpu gene. In particular, Nef proteins of all vpu-containing viruses had lost their ability to downmodulate the T cell (TCR-CD3) receptor. Here we examined Nef proteins from eight additional SIV lineages, including SIVgor, SIVwrc, SIVolc, SIVgri, SIVdrl, SIVlho, SIVden, and SIVasc, from western lowland gorillas, western red colobus monkeys, olive colobus monkeys, grivet monkeys, drills, L'Hoest's monkeys, Dent's mona monkeys, and red-tailed monkeys, respectively. We found that except for the nef gene of SIVdrl, all of them were efficiently expressed and modulated CD4, major histocompatibility complex class I (MHC-I), CD28, CXCR4, and Ii cell surface expression and/or enhanced viral infectivity and replication. Furthermore, the Nef proteins of SIVgri, SIVlho, SIVwrc, SIVolc, and SIVgor antagonized tetherin. As expected, the Nef protein of SIVgor, which carries vpu, failed to downmodulate CD3, whereas those of SIVwrc, SIVgri, SIVlho, and SIVasc, which lack vpu, were capable of performing this function. Surprisingly, however, the Nef protein of the vpu-containing SIVden strain retained the ability to downmodulate TCR-CD3, whereas that of SIVolc, which does not contain vpu, was unable to perform this function. Although the SIVden Vpu is about 20 amino acids shorter than other Vpu proteins, it degrades CD4 and antagonizes tetherin. Our data show that there are exceptions to the link between the presence of a vpu gene and nef alleles deficient in CD3 modulation, indicating that host properties also affect the selective pressure for Nef-mediated disruption of TCR-CD3 signaling. Our results are also further evidence that tetherin antagonism is a common function of primate lentivirus Nef proteins and that the resistance of human tetherin to Nef represents a relevant barrier to cross-species transmission of SIVs to humans.
Maternal human immunodeficiency virus type 1 (HIV-1) infection in sub-Saharan Africa is a major public health concern because of the high prevalence among women of childbearing age and the poor prognosis for perinatally infected children. Characteristics associated with HIV seroprevalence were studied in a population of 1,833 pregnant women seen in two large mother-child clinics in Brazzaville, Congo. The prevalence of HIV infection was 3.9% (95% confidence interval, 3.0–4.9%) and differed significantly according to the district of residence, marital status, duration of the relationship with the current partner, number of sexual partners in the year prior to pregnancy, number of living and dead children, and history of blood transfusion and/or hospitalization. Logistic regression analysis identified six significant factors independently associated with seropositivity; age, history of blood transfusion and/or hospitalization, district of residence, duration of the relationship, number of living children, and number of deceased children. However, the predictive value of the model was poor: while 80% of the truly positive women were correctly predicted positive by the model, 50% of the truly negative women were misclassified. Among pregnant women attending these clinics it is therefore difficult to identify a subgroup at risk toward which specific actions could be targeted.
The relationship between fulminant viral hepatitis (FVH) and pregnancy was compared in Algeria and France. This comparison was based on the study of 22 Algerian and 77 French pregnant and non-pregnant women, aged 15 to 49 years, consecutively admitted for FVH to the Centre Hospitalier Universitaire, Constantine, Algeria, or to Hôpital Beaujon, Clichy, France. The observed and expected (calculated from demographic data) percentage of pregnant women was significantly different among the Algerian patients with FVH (45·5% v. 24·9%, P<0·03), but not among the French patients (3·9% v. 5·8%). Hepatitis A was the cause of FVH in none of the Algerian patients, but in eight French patients, none of whom was pregnant. Hepatitis B was the cause of FVH in one non-pregnant Algerian patient and in 49 French patients, two of whom (4·1%) were pregnant. Hepatitis non-A, non-B was the cause of FVH in 21 Algerian patients, ten of whom (47·6%, a percentage significantly higher than expected, P<0·04) were pregnant, and in 19 French patients, one of whom (5·3%, a percentage similar to that expected) was pregnant. In conclusion, (1) there is a relationship between FVH and pregnancy in Algeria, but not in France, and (2) this difference is mainly or exclusively attributable to infection with a non-A, non-B virus affecting the Algerian population, but which is much less common or absent in France.
