Article information
Resumen
El paciente infectado por el virus de la inmunodeficiencia humana presenta una incidencia incrementada de episodios cardiovasculares relacionados con la arteriosclerosis. El virus es capaz de replicar en la pared arterial, lo que implica una disfunción inflamatoria severa, la cual, cuando se acompaña de los trastornos metabólicos asociados a la infección y a su tratamiento hace que la placa de ateroma presente una progresión acelerada. El virus tiene una alta replicación en los linfocitos T CD4+ que se instalan en el espacio subendotelial. Éstos producen proteínas virales com Tat que inducirán la síntesis de quimiocinas como MCP-1 o moléculas de adhesión VCAM-1. Esta combinación atraerá a monocitos para que se instalen en el espacio subendotelial que, además, penetrarán de forma más rápida cuando están infectados. También se infectarán las células musculares lisas, lo que producirá el inicio de la disfunción endotelial. La dislipemia y la resistencia a la insulina provocarán la modificación de lipoproteínas, las cuales serán fagocitadas mediante el receptores CD36 por los macrófagos del espacio subendotelial. EL transporte reverso del colesterol estará dañado, ya que la proteína viral Nef es capaz de bloquear el receptor ABCA1 de las lipoproteínas de alta densidad. Estos acontecimientos producirán un acúmulo rápido de colesterol en el núcleo de la placa de ateroma. Posteriormente, la placa se complicará, bien por rotura o por erosión. En este momento se formará un trombo yuxtalesional, donde la plaqueta se activa.
Palabras clave:
VIH
Linfocitos T CD4+
MCP-1
Ateroma
RANTES
Abstract
Patients with HIV have an increased risk of cardiovascular events related to arteriosclerosis. The virus is able to replicate in the arterial wall, implying severe inflammatory dysfunction. When this inflammatory dysfunction is accompanied by the metabolic disorders associated with HIV infection and its treatment, progression of the atheroma plaque is accelerated. HIV shows high replication in CD4+ T lymphocytes, which accumulate in the subendothelial space. CD4+ T lymphocytes produce viral proteins such as Tat, which leads to synthesis of chemokines such as monocyte chemoattractant protein-1 (MCP-1) or vascular cell adhesion molecule-1. This combination will attract monocytes into the subendothelial space, which penetrate rapidly if infected. These monocytes will also infect the smooth muscle cells, producing the initiation of endothelial dysfunction. Dyslipidemia and insulin resistance will then provoke modification of lipoproteins, which will be phagocytized through CD36 receptors by macrophages of the subendothelial space. Reverse cholesterol transport will be damaged, since the Nef viral protein is able to block the ABCA1 receptor. These events will produce rapid cholesterol accumulation in the atheroma plaque nucleus. Subsequently, the plaque will become complicated, either by rupture or erosion. Then, a juxtalesional thrombus is formed, where the platelet is activated.
Keywords:
HIV
CD4+ T lymphocytes
MCP-1
Atheroma
RANTES
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