Analysis of HIV type 1 BF recombinant sequences from South America dates the origin of CRF12_BF to a recombination event in the 1970s.

HIV-1 epidemics in South America are believed to have originated in part from the subtype B epidemic initiated in the Caribbean/North America region. However, circulation of BF recombinants in similar proportions was extensively reported. Information currently shows that many BF recombinants share a recombination structure similar to that found in the CRF12_BF. In the present study, analyzing a set of 405 HIV sequences, we identified the most likely origin of the BF epidemic in an early event of recombination. We found that the subtype B epidemics in South America analyzed in the present study were initiated by a founder event that occurred in the early 1970s, a few years after the introduction of these strains in the Americas. Regarding the F/BF recombinant epidemics, by analyzing a subtype F genomic segment within the viral gene gag present in the majority of the BF recombinants, we found evidence of a geographic divergence very soon after the introduction of subtype F strains in South America. Moreover, through analysis of a subtype B segment present in all the CRF12_BF-like recombination structure, we estimated the circulation of the subtype B strain that gave rise to that recombinant structure around the same time period estimated for the introduction of subtype F strains. The HIV epidemics in South America were initiated in part through a founder event driven by subtype B strains coming from the previously established epidemic in the north of the continent. A second introduction driven by subtype F strains is likely to have encountered the incipient subtype B epidemic that soon after their arrival recombined with them, originating the BF epidemic in the region. These results may explain why in South America the majority of F sequences are found as BF recombinants.

Lack of viral selection in human immunodeficiency virus type 1 mother-to-child transmission with primary infection during late pregnancy and/or breastfeeding.

Mother-to-child transmission (MTCT) of human immunodeficiency virus type 1 (HIV-1) as described for women with an established infection is, in most cases, associated with the transmission of few maternal variants. This study analysed virus variability in four cases of maternal primary infection occurring during pregnancy and/or breastfeeding. Estimated time of seroconversion was at 4 months of pregnancy for one woman (early seroconversion) and during the last months of pregnancy and/or breastfeeding for the remaining three (late seroconversion). The C2V3 envelope region was analysed in samples of mother-child pairs by molecular cloning and sequencing. Comparisons of nucleotide and amino acid sequences as well as phylogenetic analysis were performed. The results showed low variability in the virus population of both mother and child. Maximum-likelihood analysis showed that, in the early pregnancy seroconversion case, a minor viral variant with further evolution in the child was transmitted, which could indicate a selection event in MTCT or a stochastic event, whereas in the late seroconversion cases, the mother's and child's sequences were intermingled, which is compatible with the transmission of multiple viral variants from the mother's major population. These results could be explained by the less pronounced selective pressure exerted by the immune system in the early stages of the mother's infection, which could play a role in MTCT of HIV-1.

Asociación de la infección del timo y médula osea con el establecimiento de la infección persistente con virus Junín en dos géneros de roedores / Infection of thymus and bone marrow during the establishment of the Junin virus persistent infection in rodents

Este trabajo demuestra una correlación entre la infección productiva del virus Junín en timo y el establecimiento de la infección persistente en la rata y el ratón. Los animales fueron inoculados con 10**4 ufp por vía intracerebral. La variación de la edad de inoculación señaló que en los ratones de menor edad (menores de 24 h), que son los que presentan un porcentaje mayor de persistencia, la infección tímica fue más temprana y productiva. A su vez variando la cepa de virus Junín, en ratones de menos de 24 h, la cepa patógena XJ que normalmente produce en estas condiciones experimentales una mayor sobrevida con persistencia, alcanzó en timo niveles más altos que la cepa atenuada XJCL3. En el modelo rata de 3 días la cepa XJ provoca una mortalidad de solo el 10%, sobreviviendo el resto con infección persistente en tanto que con la cepa XJCL3 la mortalidad alcanza al 95%. En este modelo se aisló virus al 7 día pi de timo y médula ósea cuando se infectó con XJ, mientras que no se detectó en ninguno de estos órganos cuando se empleó la cepa atenuada XJCL3. En ratones inoculados dentro de las 24 h de edad y sacrificados al día 14 pi, también se pudo relacionar el desarrollo de la enfermedad con la infección tímica ya que solo en los animales que no presentan signos neurológicos fue posible detectar virus en timo. Además de la correlación entre la infección de órganos del sistema inmune y la persistencia de virus Junín en el roedor, los datos obtenidos sugieren que la regulación de la respuesta inmune es más importante que la modulación de la replicación viral en encéfalo para el establecimiento de la infección persistente