**3. Epidemiology of neurological HIV disease**

Studies on the prevalence of HIV among neurologic patients are sparse. The most often quoted study is the CDC study of 195,000 patients in 20 acute-care US hospitals, which found a seroprevalence of 0–13%. This was highly correlated with the seroprevalence among all patients in the hospitals [2]. The study data was difficult to interpret as almost two-thirds of the HIV patients were previously undiagnosed. In a hospital-based study that audited HIV manifestations in medical inpatients in South Africa, the frequency of neurological involvement was 75%, with 11% pure neurological disease, and 64% neurological and non-neurological disease combined [4].

There are several different HIV-1– clades based on phylogenetic data from the diverse HIV strains. Group M ("main") is responsible for the majority of infections worldwide, and is further divided into at least 10 distinct subtypes or clades A, B, C, D, F1, F2, G, H, J, and K. Group O ("out-group") is a relatively rare group currently found in Cameroon, Gabon, and France [6]. The different clades of HIV-1 are not distributed evenly throughout the world. Clade B dominates in North America and Europe. Clade C virus predominates in parts of Sub-Saharan Africa and Asia. Globally, clade C virus is responsible for an estimated 50% of infections and is linked to the rapidly growing epidemics in Sub-Saharan Africa and some parts of Asia,

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The effect of the different clades in different populations on the pathological spectrum of HIV infection in these populations is not known. The majority of published data on HIVassociated neurological disease relates mainly to clade B, which is found in North America, Europe, and Australia. Information from regions where clade C dominates is emerging and seems to indicate that there is no effect of the clade on the spectrum of neurological mani-

Aseptic meningitis is a clinicopathological syndrome, and the cardinal symptoms of which are headache, fever, and meningism. Pathologically, it is characterized by serous, nonpyogenic inflammation of the meninges. The defining cerebrospinal fluid (CSF) findings include a mononuclear pleocytosis, normal, or mildly raised protein and normal glucose levels [1]. Aseptic meningitis occurs with an annual incidence rate of 11–27 cases per 100,000 population. The causes are mainly viral infections. Of these, enteroviruses (Echo and Coxsackie) make up 80% of cases followed by mumps, HSV-2, lymphocytic choriomeningitis, and adenovirus. Uncommon causes include infectious mononucleosis, cytomegalovirus (CMV), leptospirosis, HSV-1, mycoplasma, arboviruses (in epidemics mainly in the United States and Europe) and rarely during the icteric phase of infectious hepatitis. In the majority of instances, a causative agent cannot be established (exceptions include enteroviruses, mycoplasma, leptospirosis, and Lyme borreliosis) [1]. The aseptic meningitis in most of these conditions is a self-limiting illness and rarely is of sufficient severity to produce pathological changes in the brain that can

It is important to recognize that an aseptic meningitis syndrome can occur in the course of other infectious and noninfectious inflammatory granulomatous and vasculitic and autoimmune illnesses. This is well described with respect to partially treated bacterial meningitis, so-called neighborhood infections, fungal, mycobacterial, spirochetal, and parasitic meningitis, malignant meningitis, and other noninfectious inflammatory diseases such as sarcoidosis, Behçet's disease, Wegener's granulomatosis, and granulomatous angiitis of the nervous system [1, 2].

mainly in India and China [6, 7].

**4. HIV-associated neurological HIV disease**

be visualized with imaging modalities (CT or MRI).

festations [4].

**4.1. Aseptic meningitis**

*4.1.1. Introduction*

The paucity of this type of data is in stark contrast to established data on the global prevalence of HIV from the Joint United Nations Programme on HIV/AIDS (UNAIDS). In 2016, the WHO estimated that 36.7 million people worldwide are infected with HIV. Sub-Saharan Africa bears the brunt of the HIV epidemic with 25.5 million infected individuals (a prevalence of 6% and 69% of all persons with HIV globally). Asia and the Pacific have 5.1 million infected people, and Latin America has 1.6 million infected people [5].

There are two principal subtypes of HIV, namely HIV-1 and HIV-2:

HIV-1, the predominant subtype is spread worldwide. HIV-2 was found predominantly in West Africa with scattered cases reported in the Americas and Western Europe. Both are associated with the clinical development of progressive immunological impairment with some differences in incubation and transmission properties. HIV-1 is the major cause of AIDS in humans [6].

There are several different HIV-1– clades based on phylogenetic data from the diverse HIV strains. Group M ("main") is responsible for the majority of infections worldwide, and is further divided into at least 10 distinct subtypes or clades A, B, C, D, F1, F2, G, H, J, and K. Group O ("out-group") is a relatively rare group currently found in Cameroon, Gabon, and France [6].

The different clades of HIV-1 are not distributed evenly throughout the world. Clade B dominates in North America and Europe. Clade C virus predominates in parts of Sub-Saharan Africa and Asia. Globally, clade C virus is responsible for an estimated 50% of infections and is linked to the rapidly growing epidemics in Sub-Saharan Africa and some parts of Asia, mainly in India and China [6, 7].

The effect of the different clades in different populations on the pathological spectrum of HIV infection in these populations is not known. The majority of published data on HIVassociated neurological disease relates mainly to clade B, which is found in North America, Europe, and Australia. Information from regions where clade C dominates is emerging and seems to indicate that there is no effect of the clade on the spectrum of neurological manifestations [4].
