Cellular AATF gene encodes a novel miRNA that can contribute to HIV-1 latency.

HIV-1 encoded microRNA hiv1-miR-H1 is known to induce CD4+ lymphopenia through its ability to downregulate cellular AATF gene. The present study directed to examine the target sites of this miRNA on AATF gene revealed the existence of a novel miRNA designated as hmiR-che-1 which had the inherent capacity to target HIV-1 genome especially regions coding for hiv1-miR-H1 as well as Vpr gene. Further, the expression of AATF gene coupled with its encoded microRNA hmiR-che-1 exhibited characteristic antagonism with the expression of hiv1-miR-H1 within the lymphocytes, derived from asymptomatic as well as symptomatic AIDS subjects. Based upon these observations, we propose that the widely recognised HIV-1 latency in CD4+ T-lymphocytes may arise, because of the orchestrated balance that may exist between the expression levels of hiv1-miR-H1 and hmiR-che-1 within lymphocytes infected with HIV-1.

Cellular & molecular basis of HIV-associated neuropathogenesis.

Although a plethora of molecules have been implicated in the development of HIV associated dementia (HAD), the identity of the indispensable ones is still elusive. The action of various molecules appears to follow a cascade path with one molecule activating another thereby regulating the expression and modulation of the regulatory machineries. Two pathways have been proposed leading to HIV-induced central nervous system (CNS) injury. First involving neurotoxic effect of viral proteins and second, with immunomodulatory substances secreted by the infected cells playing vital role. The viral transfer from infected cells (for example, cells representing macrophage-microglial lineage) to uninfected cells (such as same cell type or nerve cells) occurring perhaps via virological synapse is also not well documented. While the mechanism underlying transfer of HIV-1 through blood-brain barrier is not clearly understood, macrophage-microglial cell lineages are undisputedly predominant cell types that HIV uses for transmission in CNS. The present review describes existing knowledge of the modus operandi of HIV-induced neuropathogenesis gathered through research evidences. of HIV-induced neuropathogenesis gathered through research Mechanisms by which regulatory molecules exploit such cell types in promoting neuropathogenesis would provide key insights in intersecting pathway(s) for designing intervention strategies.

Cellular AATF gene: armour against HIV-1.

Outcome of HIV-1 infection at the cellular level is decided by the orchestrated balance that exists between cellular nucleic acid-based adaptive immune mechanism involving non-coding micro RNAs (miRNAs) and offensive tactics of HIV-1 to suppress this host cellular immunity. In this context, the review explains the importance of a novel miRNA encoded exclusively and conspicuously by HIV-1 genome that has the ability to specifically target cellular AATF gene recognized to play a crucial role in the maintenance of adaptive immunity at nucleic acid level against HIV-1 invasion.

Molecular mechanisms of HIV-1 associated neurodegeneration.

Since identification of the human immunodeficiency virus-1 (HIV-1), numerous studies suggest a link between neurological impairments, in particular dementia, with acquired immunodeficiency syndrome (AIDS) with alarming occurrence worldwide. Approximately, 60% of HIV-infected people show some form of neurological impairment, and neuropathological changes are found in 90% of autopsied cases. Approximately 30% of untreated HIV-infected persons may develop dementia. The mechanisms behind these pathological changes are still not understood. Mounting data obtained by in vivo and in vitro experiments suggest that neuronal apoptosis is a major feature of HIV associated dementia (HAD), which can occur in the absence of direct infection of neurons. The major pathway of neuronal apoptosis occurs indirectly through release of neurotoxins by activated cells in the central nervous system (CNS) involving the induction of excitotoxicity and oxidative stress. In addition a direct mechanism induced by viral proteins in the pathogenesis of HAD may also play a role. This review focuses on the molecular mechanisms of HIV-associated dementia and possible therapeutic strategies.

HAART & the molecular biology of AIDS dementia complex.

The era of highly active antiretroviral therapy (HAART) has led to a considerable decline in the HIV disease progression rates and HIV-1-related opportunistic infections especially in developed countries. Unfortunately, antiretroviral treatment for almost 90 per cent of the HIV-infected population is not available because of cost concerns. Although a number of studies have shown uniform impact of HAART on disease progression, its effect on treating HIV infection of the brain and its manifestations, such as AIDS dementia complex (ADC), remains unclear. Along with the reasons why AIDS dementia complex continues to be a problem in the era of HAART, this review also discusses the changes in ADC patterns with HAART and its relevance in developing countries such as India. In addition, an overview of various biological, molecular and therapeutic aspects that may influence HIV dementia (HIV-D) is provided.

HIV-1 Nef control of cell signalling molecules: multiple strategies to promote virus replication.

HIV-1 has at its disposal numerous proteins encoded by its genome which provide the required arsenal to establish and maintain infection in its host for a considerable number of years. One of the most important and enigmatic of these proteins is Nef. The Nef protein of HIV-1 plays a fundamental role in the virus life cycle. This small protein of approximately 27 kDa is required for maximal virus replication and disease progression. The mechanisms by which it is able to act as a positive factor during virus replication is an area of intense research and although some controversy surrounds Nef much has been gauged as to how it functions. Its ability to modulate the expression of key cellular receptors important for cell activation and control signal transduction elements and events by interacting with numerous cellular kinases and signalling molecules, including members of the Src family kinases, leading to an effect on host cell function is likely to explain at least in part its role during infection and represents a finely tuned mechanism where this protein assists HIV-1 to control its host.

HIV: transmissäo materno-fetal (revisäo) / HIV: maternal-fetal transmission (review)

O número de mulheres infectadas com o vírus da imunodeficiênicia humana vem aumentando nos últimos anos emconseqüência do uso de drogas injetáveis, múltiplos parceiros sexuais ou parceiros único HIV positivo ou em situaçöes de risco. A transmissäo materno-fetal varia de 14 a 30(pôr cento) e está relacionada com as características do vírus infecçäo primária durante a gravidez, doença materna avançada, estado imunológico da gestante, gestaçäo pré ou pós-termo e o tipo de parto. Revisamos os tipos de transmissäo mäe/filho, métodos diagnósticos e recomendaçÆes para prevençäo, incluindo o uso de Zidovudine

Productos naturales del bosque humedo tropical de Venezuela, inhibidores de la replicacion de VIH-1 / Natural products from the amazonian rainforest of Venezuela as inhibitors of HIV-1 growth

More than 100 plant extracts from the Amazonian rain forest of Venezuela were evaluated for their cytotoxicity and inhibitory activity against the human immunodeficiency virus type-1 (HIV-1). Aqueous extracts from Fomitella supina (S # 0389-4), Phellinus rhabarbarinus (S # 0389-7), Trichaptum perrottetti (S # 0389-8) and Trametes cubensis (S # 0389-13), Polyporaceae exhibited strong anti-HIV-1 activity, without toxicity for Molt-4 lymphocytic cells. Our results demonstrated, that the compound(s) acted by mechanism of direct virion inactivation and by inhibition of syncytium formation in an in vitro culture system. These results support the suggestion that the test extracts specifically act at the level of CD4-gp120 binding. The active components of these extracts is at present unknown, but anti-AIDS agents, such as those found in this study, individually or in combination, may be of therapeutic relevance

Perfil inmunológico en personas infectadas por el virus de inmunodeficiencia humana (VIH-1)

Observamos la evolución del síndrome de inmunodeficiencia adquirida en 100 pacientes remitidos al laboratorio de inmunología del Hospital San José de Bogotá, quienes resultaron seropositivos para anticuerpos contra el virus de inmunodeficiencia humana tipo I (VIH-1). Nuestro objetivo, fue analizar comparativamente el perfil inmunológico entre los diferentes estadios de la enfermedad y los sujetos normales para lograr un mejor conocimiento sobre el progreso de ésta a nivel inmunológico y obtener datos que sirvan para el pronóstico de la enfermedad en nuestro medio. Investigamos también la incidencia de anticuerpos contra Toxoplasma gondii y Treponema pallidum, así como la respuesta celular a la prueba de tuberculina (PPD). Dividimos a nuestros pacientes en tres grupos, el primero compuesto por los individuos VIH (+), agrupados según el estadio de su enfermedad en: portadores asintomáticos, 38 personas; 12 pacientes con lifadenopatía generalizada persistente y 50 con síndrome florido de SIDA. En el segundo grupo reunimos 20 personas seronegativas para anticuerpos contra el virus VIH-1, tomadas entonces como control. Por último, analizamos los datos de 28 pacientes fallecidos dentro del estudio, entre ellos también observamos en forma independiente los 16 pacientes fallecidos en los dos primeros meses posteriores a la realización de su perfil inmunológico. Analizamos las muestras de suero mediante el método de ELISA, para detectar la presencia de anticuerpos contra el virus, confirmado el resultado por la prueba de Western-blot...

In vitro HIV infection of primate lymphocytes

El propósito de este estudio fue el de evaluar la capacidad de los virus del SIDA (VIH-1 y VIH-2) para multiplicarse en las células mononuclearres de la sangre periférica (CMSP) de cuatro especies de primates. CMSP de Cebus apella, patas (Erythrocebus patas), monos verdes (cercopithecus aethiops sabeus) y rhesus (Macaca mulatta) fueron infectados "in vitro" con VIH-1 y con VIH-2. La multiplicación de estos virus se determinó midiendo la actividad de la enzima retrotranscriptasa en los cultivos infectados. Ambos virus produjeron efectos citipáticos en dichos cultivos. Se observó un bajo nivel de multiplicación de los virus VIH-1 y VIH-2 en las células provenientes de monos Cebus. Sin embargo, el virus VIH-2 se multiplicó eficientemente en CMSP de monos rhesus. La capacidad que posee el virus de la inmunodeficiencia humana tipo 2, (VIH-2) de multiplicarse en estas células, podría ser utilizada para en la evaluación "in vivo" de productos antivirales y de vacunas