Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A peptide-nucleic acid solution which had previously been reported to show in vivo efficacy in several viral infections (i.e. influenza, hepatitis, mumps, encephalitis, etc) was tested in three independent laboratories, including the US National Institutes of Health by specific in vitro methods for HIV and Influenza A. The results of these studies demonstrated significant anti-viral activity of the peptide-nucleic acid solution against the Human Immunodeficiency Virus (HIV) and the Influenza A virus.
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PMID:In vitro antiviral activity of a peptide-nucleic acid solution against the human immunodeficiency virus and influenza A virus. 172 67

Sulfated polysaccharides (i.e., dextran sulfate) and sulfated polymers (i.e., sulfated polyvinylalcohol and sulfated copolymers of acrylic acid with vinylalcohol) were found to be potent and selective inhibitors of the replication of respiratory syncytial virus (RSV) and influenza virus type A (influenza A virus) but not of other myxoviruses (parainfluenza 3, measles, and influenza B viruses). The compounds were also inhibitory to human immunodeficiency virus type 1 (HIV-1) and HIV-2 and simian immunodeficiency virus but not simian AIDS-related virus. The mode of antiviral action of the sulfated polysaccharides and polymers can be attributed to an inhibition of virus binding to the cells (HIV-1), inhibition of virus-cell fusion (influenza A virus), or inhibition of both virus-cell binding and fusion (RSV). The fact that the sulfated polysaccharides and polymers are inhibitory to some myxoviruses and retroviruses but not to others seems to depend on the composition of the amino acid sequences of the viral envelope glycoproteins that are involved in virus-cell binding and fusion. All myxoviruses and retroviruses that are sensitive to the sulfated polysaccharides and polymers share a tripeptide segment (Phe-Leu-Gly). This tripeptide segment may be involved either directly (as a target sequence) or indirectly in the inhibitory effects of the compounds on virus-cell binding and fusion.
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PMID:Differential inhibitory effects of sulfated polysaccharides and polymers on the replication of various myxoviruses and retroviruses, depending on the composition of the target amino acid sequences of the viral envelope glycoproteins. 172 92

Choosing appropriate antimicrobial therapy for patients with pneumonia requires knowledge of the etiologic agents seen in specific kinds of patients at specific times and places. For community-acquired pneumonia, there is an important difference in the agents seen in the normal and the compromised host. The normal host most often presents with viral, mycoplasmal, or pneumococcal pneumonia. The exact place of Chlamydia pneumoniae is still under study. A normal host who aspirates is at risk of anaerobic pneumonia. Normal hosts with influenza may acquire superinfection with Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus. Under specific epidemiologic conditions, community-acquired pneumonia may be due to Legionella species, Yersinia pestis, Francisella tularensis, Coxiella burnetii, Chlamydia psittaci, a mycotic agent, or tuberculosis. Patients with chronic bronchitis and emphysema are predisposed to H. influenzae, Moraxella catarrhalis, and S. pneumoniae infections. HIV-infected patients are likely to have Pneumocystis carinii pneumonia and pneumonia due to cytomegalovirus, S. pneumoniae, and H. influenzae. Patients with diabetes, nursing-home patients, hospitalized patients, immuno-compromised patients, and patients with recent antibiotic therapy are predisposed to pneumonia due to Gram-negative aerobic bacilli of enteric and environmental origin. Initial therapy should be directed at the likely organism or organisms based on hospital susceptibility surveillance. In the normal host with community-acquired pneumonia, the therapy will often be penicillin G or erythromycin. In the patient predisposed to Gram-negative pneumonia, a third-generation cephalosporin with or without an aminoglycoside is the usual choice.
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PMID:Pneumonia. Patient profiles, choice of empiric therapy, and the place of third-generation cephalosporins. 173 Jan 86

In earlier studies, primary proliferative and cytotoxic T-cell (CTL) responses to influenza virus were produced in vitro by using mouse dendritic cells (DC) pulsed with virus or viral peptide as the stimulus for syngeneic T cells in 20-microliters hanging-drop cultures. We have now adapted this system for producing primary responses with cells from non-immune donors to produce primary proliferative and CTL responses to human immunodeficiency virus I (HIV) and to HIV peptides in vitro using cells from normal human peripheral blood. All donors in this study were laboratory personnel with no history of HIV infection. DC enriched from peripheral blood were exposed to HIV in vitro and small numbers were added to T lymphocytes in 20-microliters hanging drops. Proliferative responses to virus-infected DC were obtained after 3 days in culture. After 6 days, CTL were obtained that killed virus-infected autologous--but not allogeneic--phytohaemagglutinin (PHA)-stimulated blast cells. Proliferative and CTL responses were obtained using cells from 14 random donors expressing a spectrum of major histocompatibility complex (MHC) types but the CTL, once produced, showed killing restricted by the MHC class I type. Treatment of cultures with monoclonal antibody (mAb) to CD4-positive cells at the beginning of culture blocked the development of both proliferative and CTL responses, but treatment after 5 days had no effect on the CTL activity. Treatment with MCA to CD8-positive cells at the beginning of culture did not block proliferation significantly, but treatment either before or after the 5-day culture period blocked CTL responses. Collaboration between proliferating CD4-positive cells and CD8-positive cells may thus be required to produce CTL of the CD8 phenotype. DC exposed to HIV also produced CTL that killed autologous blast cells pulsed with gp120 envelope glycoprotein. However, DC infected with whole virus did not produce CTL that lysed target cells pulsed with a synthetic peptide, which included a known T-cell epitope of gp120 (representing amino acids 111-126). DC pulsed with gp120 were a poor stimulus for the development of CTL. In contrast, DC pulsed with the peptide (111-126) stimulated both proliferative and CTL responses. The latter killed not only target cells pulsed with the peptide itself or with gp120 but also killed virus-infected autologous blast cells. CTL were again obtained reproducibly with this peptide using donors expressing a spectrum of MHC types.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Primary proliferative and cytotoxic T-cell responses to HIV induced in vitro by human dendritic cells. 176 89

We have previously reported the identification of highly conserved homologous regions located in the carboxy terminus of the HIV 1 gp41 (aa 837-844), and the amino-terminal of the beta chain of all human HLA class II antigens (aa 19-25). Murine monoclonal antibodies raised against synthetic peptides from these homologous regions bound not only to the isolated peptides, but also to "native" HLA class II molecules on cells. Screening of sera from HIV 1 infected individuals revealed high frequency of sera (35%) containing anti-class II crossreactive antibodies (CRAb), not only in AIDS patients, but also in early, asymptomatic patients. The CRAb containing sera caused potent inhibition of normal CD4-bearing cells' proliferative responses to tetanus toxoid in vitro. They could also kill class II bearing cells by ADCC. The possible contribution of these antibodies to the establishment of immunodeficiency state in HIV 1 infected individuals and/or to disease progression, was examined in two clinical studies: I. Asymptomatic patients were tested in parallel for their PBL responses to flu/tetanus, HLA alloantigens, and PHA (proliferation and IL2 production), and for the presence of anti-class II CRAb. About 50% of these patients showed a selective loss of their in vitro responses to recall antigens (flu/tetanus), which depend on CD4+ cells, while still responding to PHA and ALLO. Interestingly, positive correlation was found (P less than 0.001) between patients' lack of responsiveness to flu/tetanus and the presence in their sera of anti-class II CRAb. II. Retrospective study of HIV 1-infected hemophiliacs, suggest that patients with high titers of CRAb early in the disease progressed faster to full blown disease.
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PMID:Common sequence in HIV 1 GP41 and HLA class II beta chains can generate crossreactive autoantibodies with immunosuppressive potential early in the course of HIV 1 infection. 180 76

A case study is given of a 25-year old woman with rhabdomyolysis associated with HIV infection. The presenting symptoms were a 1-week history of backache, gross swelling of both hands and feet, and weakness and marked pain in most muscle groups; 3 days before admission the urine was black and she was unable to walk. Multiple, firm 1-2 cm lymph nodes were revealed during examination. White blood cell count (WBC) was 22,000/microliter with 12 pc lymphocytes, 7.3 pc monocytes, and 80.5 pc polymorphonuclear leukocytes. Hemoglobin concentration was 15.8 g/deciliter; platelet count was 124,000/microliter with a Westergren ESR of 109 mm/h. An antinuclear antibody test was negative. Serum concentration of urea was 3.8 mmol/liter, creatinine 42 microliter/liter, sodium 128 mmol/liter, and potassium 5.9 mmol/liter. Microscopic examination of urine revealed WBC 100/HPF, red blood cells 20/HBF, and granular casts. The dipstick test showed blood land protein in the urine. Electromyography showed inflammatory myopathy. Creatine Kinase (CK) concentration was 2359 IU/liter and lactate dehydrogenase concentration 1000 IU/liter. Hemolysis was present from clinical or laboratory signs. The patient tested HIV positive by ELISA (Abbott) and Western blot (Dupont). Treatment consisted of administration of 60 mg/day of prednisolone orally. Over 2 weeks, swelling of limbs was reduced and CK concentration was reduced to 931 IU/liter. The patient was discharged and did not keep a follow-up appointment. The patient did not have a history of other predisposing conditions, only HIV infection and persistent muscle weakness and inflammatory myopathy. There is evidence from other patient studies of myopathy associated with HIV infection and polymyositislike illness. In this case study, the patient may have had a acute form of polymyositis, or acute viral myositis such as occurs with echo, influenza, coxsackie, and other viral infections. A detailed viral investigation was not performed. HIV infection may have directly infected myocytes or immunosuppression predisposing to acute myositis by other pathogens. HIV-related muscle disease should include rhabdomyolysis.
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PMID:Rhabdomyolysis associated with human immunodeficiency virus (HIV) infection. 180 50

In the past decade, immunization rates among preschool-age children in the United States have decreased to levels lower than those in many developing countries. As a result, epidemics of vaccine-preventable diseases have occurred, especially in urban areas. Six of the infections prevented by immunization--those caused by Bordetella pertussis, Streptococcus pneumoniae, Haemophilus influenzae type B, Corynebacterium diphtheriae, measles virus, and influenza virus--frequently cause respiratory tract disease. Pneumonia in children may have subtle presentations and require special considerations depending on the age and condition of the child and the current rate of disease in the community. In addition to the epidemics occurring throughout the country, the growing number of immunocompromised children has also influenced diagnostic, treatment, and prevention considerations. These patients include children with cancer, organ transplants, congenital immune disorders, sickle cell disease, human immunodeficiency virus infection, as well as other disorders that lead to increased risk of infection. The current recommendations for routine and special childhood immunizations are reviewed in this article.
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PMID:Vaccine-preventable respiratory infections in childhood. 180 99

A 37 year old male developed fever for 20 days, along with headache, anorexia, malaise, sweating, pharyngitis, lymphadenopathy and splenomegaly. At this stage, Ag p24 was positive and anti HIV was negative. The patient recovered fully but 6 months later positive HIV titers were demonstrated by immunofluorescence and Western-blot. A retrospective diagnosis of acute retroviral syndrome was made. The difficult differential diagnosis with infectious mononucleosis, cytomegalovirus, measles, rubella, toxoplasmosis and influenza is discussed. Thus, anti HIV antigenemia should be investigated in any patient with a mononucleosis like syndrome belonging in a high risk group for AIDS, even if Paul-Bunnell-Davidson or IgG anti VCA-EB reactions are positive.
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PMID:[Acute retroviral syndrome]. 182 45

Two effects of HIV infection on human dendritic cells (DC) in vitro have been examined. The first was the stimulation of primary responses to HIV antigens in autologous lymphocytes from normal donors. When DC were exposed to HIV (10(4) TCID/10(5) cells) for up to 24 h before addition to autologous lymphocytes, a marked primary proliferative response to the virus was observed. No proliferative response was seen when the period of pre-exposure of DC to virus was extended. Cytotoxic T cells specific for HIV-infected target cells developed in stimulated cultures. The second effect of HIV infection of DC was to block responses to other antigens, such as alloantigens and the recall antigens tetanus toxoid and influenza virus. This inhibitory effect was only evident when the DC were exposed to HIV for longer than 24 h before being added to cultures. These in vitro studies suggest that infection of DC can produce both stimulatory and inhibitory responses in lymphocytes. Such effects operating through DC might underlie in vivo activity of HIV both in stimulating the proliferation of lymphocytes (e.g., in persistent generalised lymphadenopathy) and in the development of immunosuppression.
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PMID:Stimulatory and suppressive effects of infection of dendritic cells with HIV-1. 183 77

Synthetic oligodeoxyribonucleotides have been found to inhibit the replication and expression of HIV and of Influenza virus in growing tissue cultures. Nuclease resistant oligomers have been more effective than unmodified oligomers. In mouse and rat studies, labeled oligomers, on intravenous or intraperitoneal injection, leave the blood stream rapidly and enter numerous organs of the body. The half life in these organs is 24-48 hours in the case of the phosphorothioate oligomers.
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PMID:Oligodeoxynucleotide hybridization inhibition of HIV and influenza virus. 184 Dec 68


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