Biopolym. Cell. 1997; 13(4):328-334.
Віруси та клітина
Роль макрофагів і астроцитів у механізмах нейродегенерації,
викликаної інфікуванням ВІЛ-1
- Інститут фізіології ім. О. О. Богомольця НАН України
Вул. Академіка Богомольця, 4, Київ, Україна, 01024
Abstract
При захворюванні на СНІД у значної кількості хворих відбувається порушення діяльності центральної нервової системи (ЦНС),
обумовлене проникненням, вірусу імунодефіциту людини I (ВІЛ-I) через гематоещефалімний бар'єр. Це відбувається завдяки здатності ВІЛ-I-інфікованих моноцитів зв'язуватися мікроваскулярким ендотелієм, що визначає наступне проникнення вірусу у тканину мозку. Індукована ВІЛ-І патологія ЦНС супроводжується вибірковою загибеллю нейронів кори та сітківки, астроцитозом, порушенням мієлінізації нервових волокон. ВІЛ-1 безпосередньо не інфікує нервові клітини. Головну роль у розвитку патології ЦНС відіграє секреція нейротоксинів ВІЛ-1-інфікованими макрофагами. До цих нейротоксинів належать глутамат-подібні нейротоксичні молекули, вільні радикали, цистеїн, фактор активації тромбоцитів, цитокіни, ейкозаноїди, зокрема арахідонова кислота, а також неідентифіковані фактори, що виділяють активовані макрофаги, а також реактивні астроцити
Білки ВІЛ-І, зокрема поверхневий глікопротеїн gp120, також можуть пошкоджувати нейрони і змінювати функцію астроцитів. Загибель нейронів у хворих на СНІД у значній мірі може залежити від здатності gp120 обумовлювати надмірну стимуляцію НМДА рецепторів і викликати екситотоксичн порушення, а також безпосередньо впливати на астроцити, викликаючи зменшення продукування факторів росту і пригнічуючи транспортування глутамату з міжклитинного середовища.
Повний текст: (PDF, англійською)
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