High Human Immunodeficiency Virus Type 1 RNA Load in the Cerebrospinal Fluid from Patients with Lymphocytic Meningitis

Abstract

Thirty-seven matched cerebrospinal fluid (CSF) and plasma samples from 34 human immunodeficiency virus type 1 (HIV-1) -infected patients with suspected meningitis were analyzed for levels of HIV-1 RNA and markers of inflammation. Patients with tuberculous (n Å 9) or cryptococcal (n Å 6) meningitis had the highest CSF virus loads, which in many cases exceeded the levels in plasma, compared with patients with meningococcal meningitis (n Å 3), aseptic meningitis (n Å 8), tuberculoma (n Å 2), or AIDS dementia complex (n Å 4) or with normal lumbar punctures (n Å 3). CSF virus load correlated significantly with the number of infiltrating lymphocytes (r Å .60, P õ .001) but not with plasma virus load, the levels of b 2 -microglobulin in the CSF, or the integrity of the blood-brain barrier. These data suggest significant intrathecal HIV-1 replication in patients with lymphocytic meningeal infections such as tuberculous and cryptococcal meningitis.Nervous system pathology is a common manifestation of logic impairment, particularly cognitive dysfunction in AIDS dementia complex (ADC) [8 -11], few studies have looked at human immunodeficiency virus type 1 (HIV-1) infection [1,2]. The virus enters the central nervous system (CNS) early in the effects of meningeal infection on the virus load in the CSF. The aim of this study was, therefore, to assess the effect of the course of HIV-1 infection and has been shown to be present at all stages of disease, irrespective of neurologic symptoms active infection in the CNS on the HIV-1 RNA load in the CSF and to correlate this with markers of inflammation and lymphocytes were counted in blood collected in EDTA (Onyx

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

“…However, Cryptococcus neoformans induces HIV-1 replication and enhances HIV infectivity in vitro (147,267) and cryptococcal meningitis leads to an increased HIV-1 load in cerebrospinal fluid (241). It is also likely that inflammatory stimuli of any etiology, if of sufficient intensity, will upregulate HIV-1 replication in vivo.…”

“…It is suggested that induction of successive increases in systemic HIV-1 load may lead to more rapid deterioration in the already impaired immune system and may also hasten the appearance of mutant viruses that may escape the established antiviral mechanisms. The plasma HIV-1 load is a major indicator of the prognosis (229), and there is abundant evidence that exogenous immune-activating stimuli cause increases in HIV-1 replication in blood (38,41,125,234,250,255,290,319,320,326), in tissues (56,249,254,319), and in anatomical compartments (37,62,193,241,245). However, the epidemi-ological evidence to support the hypothesis that immune-activating stimuli also accelerate HIV-1 disease progression in the longer term is less clear.…”

Changing Patterns in the Neuropathogenesis of HIV During the HAART Era

“…Entry of HIV-1 into the brain involves the interaction of several factors such as HIV proteins, cytokines, chemokines, and adhesion molecules (33,88,94) and is proposed to occur early in the progression of AIDS (84,101). Patients with HIVE show tight junction disruption (18) and increased endothelial cell DNA fragmentation (107).…”

Effect of Efflux Inhibition on Brain Uptake of Itraconazole in Mice Infected withCryptococcus neoformans

“…The transport of C. neoformans through the brain and its effect on the BBB have not yet been described. Only one study by Morris et al (1998) described that of nine AIDS patients with C. neoformans meningitis, only three showed an alteration of BBB. These data suggested that, in our model, C. neoformans could provoke a rupture of tight junctions allowing ITC to cross BBB by paracellular transport without affecting transcellular transfer.…”