Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nervous system is profoundly affected by acquired immunodeficiency syndrome. Nervous system pathology is responsible for the initial symptoms in 10 percent of AIDS patients and is found at autopsy in 75 percent of patients with AIDS. Human immunodeficiency virus can directly infect the brain, producing a dementia. It can also cause aseptic meningitis, spinal vacuolar myelopathy, distal symmetric peripheral neuropathy or inflammatory demyelinating polyradiculoneuropathy. The last condition may be effectively treated with plasmapheresis. Neurologic disorders due to other infectious agents are also common in AIDS patients.
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PMID:Neurologic complications of HIV infection. 215 83

Increased concentrations of excitotoxin quinolinic acid in cerebrospinal fluid (CSF) are associated with infection with the human immunodeficiency virus (HIV-1) and have been implicated in the pathogenesis of the acquired immune deficiency syndrome (AIDS) dementia complex. In the present study, inoculation of macaques with D/1/California, an immunosuppressive serotype 1 type D retrovirus, was associated with acute and chronic increases in CSF and serum quinolinic acid concentrations in macaques that had developed SAIDS, a simian disease analogous to AIDS in humans--particularly macaques with demonstrable opportunistic infections. Kynurenic acid, an antagonist of excitatory amino acid receptors as well as the excitotoxic effects of quinolinic acid, was also increased in the CSF of SAIDS macaques, but to a significantly lesser degree than was quinolinic acid (kynurenic acid, 1.8-fold; quinolinic acid, 15.6-fold). CSF quinolinic acid, but not kynurenic acid, was also increased in viremic macaques with SAIDS-related complex (2.4-fold) and asymptomatic virus positive carriers (3.4-fold). Macaques that had recovered from D/1/California infection and were antibody positive and virus negative had normal CSF quinolinic acid and kynurenic acid concentrations. Increased activity of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway, was indicated in the macaques with SAIDS by reduced serum L-tryptophan and elevated serum L-kynurenine concentrations. Macaques infected with D/1/California may provide a primate model for investigation of the mechanisms involved in increases in CSF quinolinic acid in retrovirus and other infectious diseases, including HIV-1. It remains to be determined whether the increased CSF quinolinic acid concentrations and the increased ratio of quinolinic acid to kynurenic acid have neurological significance or are a useful "marker" of infection.
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PMID:Increased ratio of quinolinic acid to kynurenic acid in cerebrospinal fluid of D retrovirus-infected rhesus macaques: relationship to clinical and viral status. 216 38

Infection with human immunodeficiency virus Type-1 (HIV-1), the causative agent of AIDS, can be associated with central nervous system as well as immune system disease. Advanced AIDS can be complicated by a dementia. Short of frank dementia, many AIDS patients manifest neuropsychological (NP) impairment including disturbance in speeded information processing, abstraction, learning, and recall. Data conflict on whether medically asymptomatic HIV-1 carriers have subtle NP deficits. Variations in tests chosen, criterion specification, and sample selection may all be contributing to disparate results. Longitudinal research is needed, and this should examine representative samples of HIV-1 seropositive individuals for whom approximate date of seroconversion is known and in whom sources of comorbidity (e.g., drug abuse, concurrent infections, CNS injuries) can be specified.
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PMID:Human immunodeficiency virus-type 1 (HIV-1) and the brain. 218 Oct 1

Picomolar concentrations of native or recombinant coat protein gp120, from the human immunodeficiency virus type 1 (HIV-1), injured rat retinal ganglion cell neurons in culture. This form of neurotoxicity could be completely abrogated by anti-gp120 but not by control preimmune serum, suggesting that the lethal effects of the purified preparations of the envelope protein were due to gp120 and not to a contaminant. Entry of HIV-1 is mediated by gp120 binding to a surface protein, designated "CD4," which is located, for example, on T lymphocytes. However, in the present study, specific anti-CD4 antibodies, at concentrations known to block effects mediated by high-affinity binding to CD4 on the surface of rat T cells, did not prevent neuronal injury induced by gp120. These findings suggest that injury of central neurons engendered by gp120 may be responsible, at least in part, for the neurologic manifestations observed in as many as 2/3 of the patients with acquired immunodeficiency syndrome, such as dementia, myelopathy, and visual loss, even in the absence of superinfection. In contrast with previous studies, however, this report suggests that the deleterious effects of gp120 on neurons may not be mediated via binding to the CD4 molecule.
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PMID:Neuronal injury due to HIV-1 envelope protein is blocked by anti-gp120 antibodies but not by anti-CD4 antibodies. 223 33

Human immunodeficiency virus (HIV) infections are accompanied by many different types of neurological complications. Opportunistic infections and neoplasms, particularly lymphoma, are often an underlying cause for these complications in patients with acquired immunodeficiency syndrome (AIDS). Frequently, these can be detected by cerebrospinal fluid (CSF) examination, double-dose contrast transmission computed tomography (CT), and/or magnetic resonance imaging (MRI). It has become apparent that the HIV itself is responsible for a significant percentage of neurological disease in the HIV-seropositive individual. The onset may be subtle and may occur before the onset of frank immunosuppression. Diagnosis of HIV encephalitis or AIDS dementia complex (ADC) is complicated by the frequent coexistence of opportunistic infections. Structural neuroimaging (CT or MRI) shows atrophy and in some case white matter abnormalities, but imaging-pathological correlation suggests that these modalities are relatively insensitive to the presence of HIV brain infection. Functional neuroimaging, both 18fluorodeoxyglucose positron emission tomography (PET) for evaluation of glucose metabolism and 123I iodoamphetamine or 99mTc-HMPAO single-photon emission computed tomography (SPECT) for evaluation of cerebral perfusion, can demonstrate abnormalities in the subcortical gray matter structures and the cerebral cortex in patients with ADC. These abnormalities may be observed early in the course of ADC even when MRI is negative and the patient is relatively asymptomatic. Also, PET and SPECT may be useful to follow progression of the dementia or response to therapy.
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PMID:Brain imaging in acquired immunodeficiency syndrome dementia complex. 223 53

We evaluated cerebrospinal fluid (CSF) concentrations of neopterin, a putative marker of activated macrophages, in 97 subjects infected with human immunodeficiency virus type 1 who had a spectrum of neurological complications. The highest CSF neopterin concentrations occurred in those with neurological opportunistic infections, primary central nervous systems lymphoma, and acquired immunodeficiency syndrome (AIDS) dementia complex. In general, the CSF concentration of neopterin was independent of CSF cell count and blood-brain barrier disruption to albumin. In the patients with AIDS dementia complex, CSF neopterin concentrations correlated with severity of disease and decreased in conjunction with clinical improvement following treatment with zidovudine. These results suggest that CSF neopterin, although not disease-specific, may be useful as a surrogate marker for the presence of AIDS dementia complex and its response to antiviral therapy.
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PMID:Cerebrospinal fluid neopterin in human immunodeficiency virus type 1 infection. 225 66

In order to determine if brain perfusion abnormalities, which are known in patients with acquiredimmunodeficiency syndrome dementia, occur in early stages of human immunodeficiency virus infection, technetium 99m hexamethyl-propyleneamine oxime-single-photon emission computed tomography studies were performed in 20 patients infected with human immunodeficiency virus who belonged to Walter Reed stages I through IV. None of these patients demonstrated signs of dementia or severe neurological dysfunction. Pathological patterns of hexamethyl-propyleneamine oxime uptake were seen in 14 patients, seven of whom had normal results during neurological examination. Only four patients had signs of cerebral atrophy on cranial computed tomographic scan. These data suggest that subtle changes in cerebral perfusion seem to arise early in the course of human immunodeficiency virus infection and may indicate human immunodeficiency virus encephalopathy before neurological symptoms or noticeable structural damage occurs.
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PMID:Reduced cerebral blood flow in early stages of human immunodeficiency virus infection. 225 52

Infection by human immunodeficiency virus (HIV) is followed in many cases by a clinically quiescent or latent phase that appears to continue as long as host antiviral defense is intact. This has raised the possibility that certain host susceptibility factors (i.e., environmental cofactors) might influence the progression of the disease. In this study we demonstrate that morphine can function to activate HIV/LTR-CAT fusion gene (HIV-long terminal repeat-chloramphenicol acetyltransferase) when transfected into undifferentiated human SH-SY5Y neuroblastoma cells. The stimulatory effect of morphine is amplified in SH-SY5Y cells that have been induced to differentiate first with phorbol 12-myristate 13-acetate (PMA) and is much less in cells differentiated with retinoic acid (RA). Morphine does not appreciably activate HIV/LTR-CAT expression in human MOLT-3 and other T cells. Morphine activation of HIV/LTR-CAT in the SH-SY5Y cells is not reversible by naltrexone and appears to involve a Fos/Jun signaling system. Our results suggest that narcotics such as morphine may lead to activation of latent HIV infection. This may be particularly important in tissues, such as brain, which can host latent HIV infection and which is uniquely damaged in patients with acquired immunodeficiency syndrome (AIDS) as evidenced by neuronal degeneration and dementia. We also predict that these findings may have important implications for the pathogenesis of AIDS, particularly in opiate drug abusers.
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PMID:Morphine-induced transactivation of HIV-1 LTR in human neuroblastoma cells. 225 36

Atrophy and white matter changes seen on magnetic resonance imaging scans have been observed in association with the acquired immunodeficiency syndrome dementia complex, but these appear to be late findings relative to clinical expression. We report a new magnetic resonance imaging observation in patients with early cognitive impairment due to human immunodeficiency virus infection. Fifty-two patients had a total of 86 magnetic resonance imaging scans during the study period. All scans were obtained with a 1.5-T system. The proton density spin echo (repetition time of 2000 milliseconds and echo delay time of 30 milliseconds) study demonstrated high-signal lesions in the region of the splenium of the corpus callosum and in the crura of the fornices. The lesions demonstrated no contrast enhancement with gadopentate dimeglumine. Pathological examination was performed in five patients. The fornix-subcallosal abnormality may be related to the memory dysfunction in patients with human immunodeficiency virus-related cognitive impairment.
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PMID:Magnetic resonance imaging findings in HIV cognitive impairment. 234 91

There are five known human retroviruses: human T-lymphotropic virus-I (HTLV-I), HTLV-II, HTLV-V, human immunodeficiency virus-1 (HIV-1), and HIV-2. These are related to animal lentiviruses. The simian retroviruses, simian T-lymphotropic virus-I (STLV-I) and STLV-III are related closely to HTLV-I and HIV-2 respectively. HTLV-I and HTLV-II and, possibly, HTLV-V are transforming agents that immortalize the CD4 cell. In contrast, HIV-1 and HIV-2 cause this cell to lyse, resulting in immunodeficiency (ID). HIV-1 and HIV-2 cause severe ID resulting in acquired immunodeficiency syndrome (AIDS). In HTLV-I and HTLV-II, ID is less severe and rarely progressive. Both of these retroviruses induce proliferation of CD4 cells. In HTLV-I, this results in acute T cell leukemia and mycosis fungoides (MF) with hypercalcemia. HTLV-V produces a less severe form of MF without hypercalcemia. Associated lymphomas (AL) occur with HTLV-I. HIV-1 and HIV-2 produce AL as well as Kaposi's sarcoma. Both also cause subcortical dementia because they are neurotropic. All human retroviruses appear to be transmitted sexually and by blood. Transfusional AIDS may be almost entirely eliminated by serologic testing of the blood supply, and transfusional lymphoma can be almost entirely eliminated by universal testing for HTLV-I.
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PMID:Human retroviruses: a common virology. 252 May 46


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