Herpes Viral Encephalitis And Multiple Sclerosis

■ Human Immunodeficiency Virus (HIV) Infection

Pathogenesis. HIV type 1 (HIV-1) is found worldwide, HIV-2 mainly in western Africa and only rarely in Europe, America, and India. HIV is transmitted by sexual contact, by exposure to contaminated blood or blood products, or from mother to neonate (vertical transmission). It is not transmitted through nonsexual contact during normal daily activities, by contaminated food orwater, orby insect bites. In industrialized countries, the mean incubation period for HIV is 9-12 years, and the mean survival time after the onset of acquired immunodeficiency syndrome (AIDS) is 1-3 years. In primary infection (transmitted through mucosal lesions, etc.), the free or cell-bound organisms enter primary target cells in the hematopoietic system (T cells, B cells, macrophages, dendritic cells), CNS (macrophages, microglia, astrocytes, neurons), skin (fibroblasts), or gastrointestinal tract (goblet cells). After replicating in the primary target cells, the virions spread to regional lymph nodes, CD4+ T cells, and macrophages, where they replicate rapidly, leading to a marked viremia with dissemination of HIV to other target cells throughout the body. About 7-14 days after this viremic phase, the immune system gains partial control over viral replication, and seroconversion occurs. The subsequent period of clinical latency is characterized by a steady rate of viral replication, elimination of HIV by the immune system, and the absence of major clinical manifestations for several years. Eventually, the immune system fails to keep up with the replicating virus, various immune functions become impaired, and the CD4+ T-lymphocyte count declines sharply. The rising viral load correlates with the progression of HIV infection to AIDS. In the nervous system, HIV initially appears in the CSF, but is later found mainly in macrophages and microglia. Symptoms and signs. Neurological manifestations can occur at any stage of HIV infection, but usually appear only in the late stages of AIDS. One-half to two-thirds of all HIV-positive individuals develop neurological disturbances as a primary or secondary complication of HIV infection or of a concomitant disease. Primary HIV infection. Early manifestations at the time of seroconversion are rare; these in clude acute reversible encephalitis or aseptic meningitis (p. 234), cranial nerve deficits (especially facial nerve palsy), radiculitis, or myelitis. Neurological signs are usually late manifestations of HIV infection. HIV encephalopathy progresses over several months and is characterized by lethargy, headache, increasing social withdrawal, insomnia, forgetfulness, lack of concentration, and apathy. Advanced AIDS is accompanied by bradyphrenia, impaired ocular pursuit, dysarthrophonia, incoordination, myo-clonus, rigidity, and postural tremor. Incontinence and central paresis develop in the final stages of the disease. CT of the brain reveals generalized atrophy, and MRI reveals multifocal or diffuse white-matter lesions. The CSF examination may be normal or reveal a low-grade pleocytosis and an elevated protein concentration. EEG reveals increased slow-wave activity. Other neurological manifestations include HIV myelopathy (vacuolar myelopathy), distal symmetrical polyradiculoneuropathies, mononeuritis multiplex, and polymyositis. Secondary complications of HIV infection include opportunistic CNS infections (toxoplasmo-sis, cryptococcal meningitis, aspergillosis, progressive multifocal leukoencephalopathy, cy-tomegalovirus encephalitis, herpes simplex encephalitis, herpes zoster, tuberculosis, syphilis), tumors (primary CNS lymphoma), stroke (infarction, hemorrhage), and metabolic disturbances (iatrogenic or secondary to vitamin deficiency). Virustatic treatment. Antiretroviral combination therapy (HAART: highly active antiretrovi-ral therapy).

HIV replication (lymph node)

HIV replication (lymph node)

Herpes Simplex Encephalitis

Release of virions

Adsorption v (virus gp120 + CD4+ receptor)

Viral penetration -Co-receptor

Release of virions

Adsorption v (virus gp120 + CD4+ receptor)

Viral penetration -Co-receptor cells/ml)

-Protein synthesis, mRNA' processing of gp160, translation envelope, capsid

Pathogenesis of HIV infection (*rT = reverse transcriptase) HIV-1 RNA

- Early manifestation, viremia, dissemination c°pies/m| p|asma)

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