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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A computer graphics molecular model of the C terminus of gp120 of HIV has been constructed using predicted secondary structure based on homologies with proteins for which X-ray crystallographic data have been published. The model shows sequences known to be important in CD4 binding in close proximity to regions with a high probability of forming alpha helical and beta strand motifs. The orientation adopted by these domains approximates to the known 3D structure of HLA-A2 alpha 2 chain without constraints based on HLA-A2 as a template being introduced. The model may therefore represent an energetically favourable conformation for a part of gp120 which mimics the binding domain for the T-cell receptor on MHC molecules. Recognition of gp120 as an alloepitope in high affinity association with CD4 would explain many of the sequelae of acquired immune deficiency on HIV infection.
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PMID:A proposed molecular model for the carboxy terminus of HIV-1 gp120 showing structural features consistent with the presence of a T-cell alloepitope. 172 16

Neurologic abnormalities occur frequently in children with symptomatic HIV-1 infection (class P2) and include cognitive, language and motor deficits, as well as acquired microcephaly. Neurologic abnormalities can be seen as early as the first 3 months of age and can precede signs of immune deficiency and systemic illness. Hypotonia, delayed or poor head control and decreased vocalizations are some of the early neurologic manifestations of HIV-1 infection. In the majority of cases CNS impairment appears to be related to HIV-1 brain infection although at this time the exact timing of CNS invasion by the virus and the pathogenesis of CNS dysfunction are unknown. Treatment with antiretroviral agents can at least temporarily improve neurologic functioning in some children with HIV-1-related encephalopathy.
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PMID:Neurologic complications of HIV infection in children. 181 29

Central nervous system findings in 30 fatal cases of human immune deficiency viral (HIV) infection are described. Twenty seven patients had acquired immune deficiency syndrome (AIDS) and three patients had serological evidence of HIV infection only (HIV seropositive). Twenty nine patients had neuropathologic abnormalities at autopsy and frequently had more than one neuropathologic process. Neurologic disease was the dominant clinical feature in nineteen patients. The spectrum of neuropathologic disease is similar to that described in other series encompassing direct HIV infection of brain; indirect CNS involvement by opportunistic pathogens differing slightly from other series in their relative frequency; lymphoma and neurovascular disease. This, the first report which serves to document the level of neurologic disease in Irish patients with AIDS and HIV infection should help to provide meaningful information for use in the planning of neurologic and rehabilitation services for these patients.
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PMID:Neuropathologic findings in AIDS and human immunodeficiency virus infection--report on 30 patients. 182 95

AIDS is an acquired immunodeficiency syndrome caused by the lentivirus HIV and characterized by a successive depletion of CD4 helper/inductor lymphocytes. The humoral and cellular immune deficiency is the basis for the development of opportunistic infections and tumors. Because of a multitude of different bacterial, viral, and parasitic opportunistic agents, AIDS is typified by a number of divergent clinical symptoms. As with many lentiviruses, HIV is difficult to demonstrate in the organism, especially in asymptomatic carriers. Although the rate of infection in peripheral lymphocytes appears to be low, there is an increasing amount of virological and immunological data which help to explain the slow but irreversible failure of the immune defense. We still know relatively little about the pathogenic mechanisms of HIV, although a number of the presently available experimental results provide useful starting points for subsequent investigations. Peter H. Duesberg recently published that HIV and AIDS may well be correlated, but stated that HIV is not the cause of AIDS. Duesberg bases his hypothesis on the fact that HIV fulfills neither Koch's classic postulates nor several more of his own postulates for viral pathogenesis. Following the summary of individual pathogenic mechanisms of HIV infection, the separate points of Duesberg's hypothesis are discussed in detail. It is made very clear that the magnitude of epidemiologic, clinical, and experimental observations and results argue for a causal role of HIV and AIDS.
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PMID:Does HIV cause AIDS? An updated response to Duesberg's theories. 198 Jun 75

In the present paper we analyze the role of major histocompatibility gene products, the human leukocyte antigens, in the pathophysiology of the acquired immunodeficiency syndrome. No association has been found between human leukocyte antigen (HLA) frequencies and human immunodeficiency virus type 1 (HIV 1) infection, whereas significant associations have been reported in some populations between some HLA haplotypes and the appearance of either opportunistic infections or secondary cancers. With regard to the human leukocyte class I antigens, their role as restriction elements in presenting HIV 1 to virus-specific cytotoxic T lymphocytes seems to be established. An increase in the serum levels of their soluble forms that correlate with disease stage has also been demonstrated. These circulating molecules could interfere with the immune response to HIV 1 and could contribute to the development of the immunodeficiency. Antigenic similarities have been detected between human leukocyte class II antigens and HIV 1 envelope proteins. These homologies could explain both the presence in some HIV-positive sera of anti-HLA class II antibodies that mediate the lysis of CD4(+)-HLA class II+ T cells and the false-positive reaction of some HIV-negative sera, which contain anti-HLA class II antibodies, in tests for HIV 1 antibodies. Reduced levels of some complement factors (the human leukocyte class III antigens) have been detected in HIV-infected subjects. These defects could play a role in the progression of the disease and affect both the clearance of HIV 1 and complement-mediated antibody responses. The data reported in this review suggest that HLA antigens may be involved in several steps of the immune deficiency of HIV-infected subjects and thus contribute to the pathophysiology of acquired immunodeficiency syndrome.
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PMID:Major histocompatibility gene products and human immunodeficiency virus infection. 199 62

Two hundred eleven HIV-seropositive patients with AIDS, AIDS-related complex, or a CD4+ cell count less than 200 x 10(6) were examined for the presence of hepatitis B virus markers during the course of their HIV infection (median follow-up of 18 months; range of 1 to 107 months). Anti-HBs was detected initially in 138 patients (65%). Sixteen patients (8%) were HBsAg positive at entry. Fourteen had chronic HBV infection of whom 12 initially were positive for HBeAg and HBV DNA; 11 remained positive during follow-up, whereas one seroconverted to anti-HBe and lost HBV DNA. Two patients with chronic HBV infection were initially negative for HBeAg and HBV DNA: one later had reactivated HBV replication and one cleared HBeAg following onset of hepatitis D infection. The last two HBsAg-positive patients had resolving acute HBV infection. Six of the 57 patients who initially were negative for HBV markers acquired HBV infection during follow-up. Four of these six patients developed chronic infection whereas two patients had acute subclinical resolving hepatitis. In addition, four patients became HBsAg positive with their last serum samples, possibly indicating reactivation of HBV infection following progressive immunological and clinical deterioration. None of the patients developed clinical symptoms that could be ascribed to HBV infection, and transaminase elevations were only sporadically recorded. It is concluded that acquisition of HBV infections is not infrequent in HIV-seropositive patients with immune deficiency. Furthermore, the course of both previously established chronic HBV infection and newly acquired HBV infection is modified in such patients, whereas reactivation of past HBV infection seems to be a rare event.
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PMID:High incidence of hepatitis B infection and evolution of chronic hepatitis B infection in patients with advanced HIV infection. 200 76

Changes in mycobacterial disease mortality between 1980 and 1986 were examined among New Jersey residents aged 25 to 44 using single cause of death data. The demographic group with the highest cumulative incidence of acquired immune deficiency syndrome (AIDS) (non-white residents of the four urban counties adjacent to New York City) sustained an increase of 10.1 deaths/100,000 men/yr and 3.1 deaths/100,000 women/yr. Groups with lower cumulative incidence of AIDS sustained smaller increases in mycobacterial disease mortality. The group with the lowest cumulative incidence of AIDS (white residents outside the four urban counties adjacent to New York City) sustained the smallest increase in tuberculosis (TB) mortality. Using single cause of death data, it was not possible to identify a relationship between increased extrapulmonary TB deaths and AIDS cumulative incidence, but such a relationship was identifiable from multiple cause of death data. Of 30 mycobacterial disease deaths of all ages with cellular immune deficiency as a contributory diagnosis on the death certificate, 21 (70%) were known to the state's AIDS registry as AIDS cases and four more (13%) were known to the registry as having human immunodeficiency virus (HIV) disease not meeting the full clinical criteria for AIDS. Young populations with a high cumulative incidence of AIDS have experienced substantially increased mortality from mycobacterial diseases. The association of mycobacterial disease mortality with HIV disease may be underestimated from AIDS registry data and from searches of single cause of death data for mycobacterial disease deaths.
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PMID:Cumulative AIDS incidence and altered mortality from mycobacterial disease: New Jersey. 200 83

Clinical and nephropathologic findings in autopsy material from 7 children with acquired immune deficiency syndrome (AIDS), 13 with severe combined immune deficiency (SCID), and 6 with a variety of other congenital immune deficiencies were reviewed in an effort to understand better the pathophysiology of the AIDS-related nephropathy. Non-HIV viral infection seemed to be associated with the development of the pathologic changes considered to be components of the AIDS-related nephropathy, and these changes, including focal segmental glomerulosclerosis (FSGS) and tubular epithelial cell injury and ectasia, were not limited to the kidneys of children with AIDS but were present in many of the congenital immune deficiencies. Of the 5 children with congenital AIDS, only the 3 who survived longer than a year developed AIDS-related nephropathy, whereas the two children with transfusion-acquired AIDS did not develop renal disease despite surviving for several years after initial infection.
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PMID:Pathology of the kidney in childhood immunodeficiency: AIDS-related nephropathy is not unique. 201 93

Changes in immune competent tissues of the HIV-1-infected person reflect to a certain extent the kind and intensity of immunological dysregulations. The diagnostic approach, however, must include immunophenotyping of cells, immunovirological studies of virus distribution in diseased tissues, and functional tests in addition to classical morphology. The latter technique alone just serves as a crude screening method since structural lesions in lymphoid tissues do not permit discrimination from other HIV-independent immune deficiency and autoimmune disorders. Although the overall appearance of lymph nodes in HIV infection and in chronic autoimmune disorders, such as collagen vascular diseases (e.g., rheumatoid arthritis and systemic lupus erythematosus), is similar, immunophenotyping shows a progressive loss of CD4 cells in HIV infection yet a quantitative increase in this cell population in autoimmune disorders (Krueger 1985a). In addition, there are other persistent active infections by lymphotropic viruses (e.g., EBV or HHV-6) which can cause structural and cellular changes in lymphoid tissues closely resembling HIV-induced lesions (Krueger et al. 1988b; Krueger 1985b). The pathological diagnosis therefore nedds to be supplemented by serological studies and--in selected cases--by in situ hybridization for the demonstration of viral genome. Southern blotting for viral DNA can only detect high numbers of viral genome copies in tissue extracts, not in which cell population the virus resides (e.g., malignant cells vs associated "normal" cells), while the polymerase chain amplification reaction, the most sensitive of all (Buchbinder et al. 1988), cannot yet differentiate between latent and (disease-related) active infection. Taking into consideration the above-described precautions in the evaluation of lymphatic lesions, there are a number of characteristic changes which reflect well the sequelae of HIV infection itself and of the ensuing immune dysregulation. Progressive loss of CD4 cells in the paracortex of lymph nodes and in the peripheral blood leads to inversion of the CD4/CD8 ratio. Loss of demonstrable CD4 cells is probably the consequence not only of cell lysis by HIV-1 infection (note: discrepancy between HIV-1 genome positive cell numbers and depletion of CD4 cells) but also of decreased CD4 marker synthesis in infected cells (Stevenson et al. 1987). In this context it is interesting that Fouchard et al. (1986) were able to show HIV expression in CD8 cells and theorized that these developed from infected CD4 cells which subsequently lost the CD4 epitope and expressed CD8.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunological dysregulation of lymph nodes in AIDS patients. 204 8

The incidence of lymphomas in individuals infected with the human immunodeficiency virus has increased progressively since the beginning of the acquired immunodeficiency syndrome (AIDS) epidemic. The present series includes 111 patients, all diagnosed and studied at one hospital in New York City. There were 108 men and three women; the average age was 39 years and male homosexuality was the predominant risk factor. The materials examined originated from 138 surgical specimens and 24 autopsies. There were 11 cases of Hodgkin's lymphoma and 100 cases of non-Hodgkin's lymphomas (NHL), a proportion strongly skewed in favor of the latter. Hodgkin's lymphoma in AIDS patients was characterized by advanced clinical stage, high histologic grade, and frequent bone marrow involvement. Non-Hodgkin's lymphoma in AIDS patients, in contrast to the general population, originated predominantly in extranodal locations (61 cases) versus locations in which the lymph nodes were the site of the primary tumors (39 cases). In the digestive tract, the unusual oral and anal primary locations were often noted and were possibly related to specific risk factors. There were 15 cases of NHL of the central nervous system, an incidence 14 times greater than that recorded in the general population. The majority of NHLs were of high histologic grade, Burkitt's and large cell immunoblastic, representing most of the cerebral and gastrointestinal tumors. All NHLs were of B-cell immunophenotype. Lymphadenopathies with the histologic features of human immunodeficiency virus infection, particularly of the late stage (type C), often preceded NHL. Probing for Epstein-Barr virus genome was more frequently positive in Hodgkin's lymphoma than in NHL. Immunologic evaluations showed severely depressed T cell counts and CD4 to CD8 cell ratios as well as markedly increased levels of antilymphocyte antibodies. Reflecting the background of profound immune deficiency, the AIDS-associated lymphomas were characterized by high aggressiveness, early tendency to generalization, frequent post-treatment relapse, and short periods of survival.
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PMID:Acquired immunodeficiency syndrome-associated lymphomas: clinical, pathologic, immunologic, and viral characteristics of 111 cases. 207 Nov 12


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