RESUMO
In this review, we describe and discuss the genetic factors that, up to some point, determine resistance to the infection and control the progression of the disease in HIV-infected individuals. Genetic factors may account for non-progression or slow progression of the disease in some of so called long-term non progressors HIV-infected individuals. In general, this group shows no symptoms for more than 10 years, while their circulating T CD4+ cells levels remain stable and they usually have a low virus load. Even though non-progression and rapid progression phenomenon are still not fully understood, there probability exists that some class I and class II MHC alleles are associated with a greater or smaller risk to develop AIDS. Class I HLA-B*35 and Cw*04 alleles are the ones commonly associated with the rapid transition of the infection into AIDS. In contrast, heterozygosity for class I HLA alleles and, particularly, the absence of HLA-B*35 and Cw*04 may contribute to non-progression. Studies which set forward other HLA alleles as possibly taking part of the pathogenic mechanism of non-progression are also described; although, relevant methodological problems can be noticed. Furthermore, this review explains and discusses allelic variations for some of the components of the chemokine receptors family, particularly the genes which codify for CCR5 and CCR2 and other genetic factors such as the SDF1-3'. A variant of the alpha SDF1 chemokine gene that have been associated with AIDS' slow progression or non-progression in HIV-infected individuals. As a whole, the factors described in this review are those that influence the natural history of the disease due to HIV and give an example of what genetic or multigenetic influence can have over the pattern of evolution of HIV infection. Finally, we mention the possible implications that the identification of the genetic markers has in the pathogenesis of HIV disease and in the development of the new therapeutic strategies to control or eliminate HIV.
Assuntos
Síndrome da Imunodeficiência Adquirida/genética , Infecções por HIV/genética , Síndrome da Imunodeficiência Adquirida/tratamento farmacológico , Síndrome da Imunodeficiência Adquirida/etiologia , Citocinas/fisiologia , Progressão da Doença , Infecções por HIV/tratamento farmacológico , Infecções por HIV/etiologia , Humanos , Complexo Principal de Histocompatibilidade/genéticaRESUMO
Se realizó un estudio descriptivo-prospectivo a 2,388 embarazadas que acudieron al Centro Materno Infantil San Lorenzo de los Mina, Santo Domingo, República Dominicana, durante el período agosto-septiembre 1988, para determinar la incidencia, el diagnóstico y tratamiento de Ruptura Prematura de Membranas. Solo 288 casos (12//) presentaron Ruptura Prematura de Membranas. En 280 (97//) casos se diagnostica Ruptura Prematura de Membranas por el método clínico; 258 (89.5//) casos por interrogatorio y exámen físico. En 155 (54//) casos fue manejado conservadoramente; 133 (46//) casos de manera agresiva; el parto vaginal fue la vía de desembarazo en 74 (65.6//) casos, y la cesárea en el 99 (34//) casos. El método clínico es altamente específico para diagnosticar Ruptura Prematura de Membranas, el manejo conservador se usó más en ambarazadas a término y pretérmino, en los inmaduros y post-maduro se indicó manejo agresivo