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Biomedical subjects

J L Sever

Publications and source records attributed to J L Sever.

At least 37 records · Page 2Linked to original sources
PubMed1989

HIV: biology and immunology.

The HIV virus grows in lymphocytes, monocyte-macrophages and possibly a few other cells of the human body. This is an RNA virus that attaches at the CD4 receptor, enters the cell, and makes DNA by using a reverse transcriptase enzyme. The virus is about 100 nm in diameter and expresses several surface and core antigens. Growth of the virus in the helper (T4) lymphocytes results in destruction of these cells. This, in turn, results in loss of cellular immune functions that causes susceptibility to infections and malignancies. Monocyte-macrophage cells are also infected but these cells are not lysed. Antigen to HIV appears in blood a few weeks after infection but disappears as antibody begins to be present. Antibody can be detected by a variety of tests but ELISA and Western blot assays are used most frequently. New latex and other methods are being licensed for use under certain circumstances.

Acquired Immunodeficiency Syndrome↗
PubMed1988

AIDS and neurological disorders: an overview.

Neurological disease occurs frequently in patients infected with the human immunodeficiency virus. Disorders may affect either the central or peripheral nervous systems and may be the presenting manifestation of human immunodeficiency virus-related disease. Opportunistic infections and lymphomas are major causes of central nervous system disease. Increasingly, however, human immunodeficiency virus infection of the central nervous system is being recognized and is now associated with a syndrome of progressive dementia in adults, referred to as the acquired immunodeficiency syndrome dementia complex, and an encephalopathy in infants born to human immunodeficiency virus-infected mothers. Whether brain disease related to this virus will respond to antiretroviral drugs will be a major focus of future research. Although less frequent than central nervous system disease, disorders of the peripheral nervous system are increasingly being recognized, including cases that probably have an autoimmune basis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Treatment of human immunodeficiency virus-related polyneuropathy with 3'-azido-2',3'-dideoxythymidine.

A 72-year-old woman with human immunodeficiency virus (HIV)-related axonal polyradiculoneuropathy of the lower extremities was treated with 3'-azido-2',3'-dideoxythymidine (AZT), 250 mg every 4 hours. Before therapy she had rapidly progressive weakness in both legs and when treatment began she could move only her toes. Six weeks after therapy, there was mild improvement in her strength, which peaked 2 months later. At her best, she was able to lift her leg 30 degrees off the bed and stand with assistance. Improvement, which was also demonstrated electrophysiologically, was short lived and partially declined when AZT was discontinued. This case demonstrates that some patients with HIV-related axonal neuropathies even in advanced stages can show objective signs of improvement when given AZT. A systematic trial with AZT in the treatment of patients with HIV-related polyneuropathies is therefore warranted.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Tropical spastic paraparesis: clinical, immunological, and virological studies in two patients from Martinique.

Two patients from Martinique with tropical spastic paraparesis had antibodies to human T-lymphotropic virus type I (HTLV-I) in serum and spinal fluid but no antibodies to other retroviruses tested. They presented with spastic weakness of both lower extremities, hyperreflexia with upgoing toes, sphincteric dysfunction, and normal sensation. By means of agarose isoelectric focusing and selective immunoblotting we demonstrated an increased intrathecal synthesis of IgG antibodies to HTLV-I in the spinal fluid. Unique oligoclonal bands of IgG antibodies to HTLV-I were present in the cerebrospinal fluid. Using a battery of monoclonal antibodies we also found in these patients an increased number of circulating T cells that expressed activation markers. We conclude that the HTLV-I retrovirus associated with tropical spastic paraparesis has both lymphocytotropic and neurotropic properties.

Adult↗
PubMed1988

Antibody to human and simian retrovirus, HTLV-I, HTLV-II, HIV, STLV-III, and SRV-I not increased in patients with multiple sclerosis.

We have tested sera from patients with multiple sclerosis, matched controls, and those with other neurological diseases, as well as sera from patients with the acquired immunodeficiency syndrome and controls and patients with tropical spastic paraparesis (TSP) and controls for antibody to human T-lymphotropic virus type I (HTLV-I), HTLV-II, human immunodeficiency virus (HIV), simian T-lymphotropic virus type III, or simian retrovirus type I by immunofluorescent activity test, and for HTLV-I and HIV by the ELISA method. Sera from patients with multiple sclerosis and matched controls, and from patients with optic neuritis and Parkinson's or other neuromuscular diseases did not have antibody to any of the retroviruses tested. Specimens from TSP patients and some controls contained HTLV-I antibody. We conclude from our study that only TSP patients had serological evidence of infection with one of the retroviruses studied.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Risk of adverse outcomes of pregnancy after human parvovirus B19 infection.

Human parvovirus B19 (B19) infection during pregnancy has been associated with fetal deaths. We conducted several studies to develop data needed to make recommendations for preventing fetal death associated with infection. In the first study, after an outbreak of B19 infection, specimens of cord blood from 47 infants with congenital anomalies, 10 with suspected intrauterine infection, and gestational age-matched controls were tested for IgG and IgM antibodies to B19. None had evidence of recent infection. Next, 192 women with unknown exposure to B19 who had stillbirths or spontaneous abortions were studied. Two patients and two controls had evidence of recent B19 infection. In a second case-control study of women who had stillbirths after outbreaks of erythema infectiosum in area schools, none of the 20 patients or 26 controls were IgM positive at the time of delivery. The rate of infection, as demonstrated by IgM positivity, among 267 pregnant control subjects was approximately 1%. These studies suggest that among pregnant women unselected for exposure to B19, neither infection nor stillbirths are common.

Antibodies, Viral↗
PubMed1988

Multiple sclerosis in the Faroe Islands. IV. The lack of a relationship between canine distemper and the epidemics of MS.

Clinical onset of multiple sclerosis (MS) occurred in 32 native resident Faroese between 1943 and 1973, comprising 3 consecutive epidemics of decreasing frequency. Relationship of MS with the appearance of canine distemper (CD) was explored by serologic studies, questionnaires, and veterinarian reports. Tested were sera from 12 MS patients and 112 controls among the 22 patients and 192 controls with questionnaires in 1978-1979. The daily treatment ledgers of the Veterinarian of the Faroes 1940-1961 were also reviewed and additional Faroese interviewed 1987-1988 as to CD. History of CD was determined for residence of all 32 MS. There was no evidence of elevated CD antibody titers in MS vs controls for neutralizing titers or ELISA values, nor to ELISA for measles. In the questionnaires only one patient and 2 of his sibs reported owning (the same) dog(s) with CD during the war. One other patient reported a possibly sick dog but not CD. CD occurred in one southern village 1941-1942, was present on Vágar from 1941-1950, and was epidemic on Streymoy 1944-1945 with scattered cases there and elsewhere through 1950. There was no significant correlation between villages with CD and MS residents. We conclude that the occurrence of multiple sclerosis was not related to the presence of canine distemper or sick dogs in the Faroe Islands.

Animals↗
PubMed1988

Avidin-biotin latex agglutination assay for detection of antibodies to viral antigens.

A new method for attaching antigens to latex by an avidin-biotin technique is described. The procedure permits control of the amount of antigen attached to the latex and eliminates the need for highly purified antigens and destructive bridging chemicals. The avidin-biotin latex agglutination assay is a simple, rapid test well suited to detection of viral antibody. The sensitivity and specificity, respectively, of the avidin-biotin latex agglutination assay compared with other assay results for antibody to viruses were as follows: cytomegalovirus, 98 and 100% (indirect hemagglutination assay); measles virus, 96 and 100% (enzyme-linked immunosorbent assay); and herpes simplex virus, 78 and 100% (indirect hemagglutination assay).

Animals↗
PubMed1988

Humoral and cellular immune responses to matrix protein of measles virus in subacute sclerosing panencephalitis.

The immune response to matrix (M) protein of measles virus was examined in patients with subacute sclerosing panencephalitis (SSPE) and controls. Antibodies specific for M and nucleocapsid (NC) proteins in 11 serum and 8 cerebrospinal fluid (CSF) samples from patients with SSPE were quantitated by enzyme-linked immunosorbent assay by using affinity-purified measles virus proteins. Geometric mean anti-NC antibody titers were higher in the serum (6.58 +/- 0.98 [mean +/- standard deviation]) and CSF (4.38 +/- 0.74) of SSPE patients compared with controls. Anti-M antibodies were present in the serum and CSF of all SSPE samples tested but in titers lower than those of anti-NC antibodies. Geometric mean anti-M antibody titer was 3.35 +/- 0.53 in sera from patients with SSPE compared with 3.05 +/- 0.66 in sera from patients with other neurological diseases and 3.12 +/- 0.74 in sera from healthy individuals. Geometric mean anti-M antibody titer was 2.59 +/- 0.86 in the CSF of eight patients with SSPE compared with a mean less than 1.00 for patients with other neurological disease (controls). Intrathecal synthesis of anti-M or anti-NC antibodies was established in four patients with SSPE. The cellular immune responses to M, F, HA, and NC proteins were examined in four of the patients with SSPE by lymphoproliferation and were not significantly different from those in five healthy controls. The results demonstrate humoral and cellular immune responses to M protein in patients with SSPE and indicate that it is unlikely that a defect in the immune response to this virus component accounts for the disease process in the patients studied.

Adolescent↗
PubMed1988

Serologic studies of MS patients, controls, and patients with other neurologic diseases: antibodies to HTLV-I, II, III.

We have studied the frequency of human retrovirus antibody (HTLV-I, II, III) in the serum and CSF of patients with MS, matched controls, and patients with optic neuritis, idiopathic and postencephalitic Parkinson's disease, neuropathies, polymyositis, ALS, and postpoliomyelitis. Except for the postpoliomyelitis samples, all samples were collected prior to 1980. Contrary to a previous published report, no significant levels of antibody to HTLV-I, II, or III were found in the MS patients or controls. No retrovirus antibody was detected in patients with the other neurologic diseases.

Antibodies, Viral↗
PubMed1988

Herpesvirus infections in pregnancy: risks to embryo, fetus, and neonate.

Gestational herpesvirus infections can significantly alter the outcome of pregnancy. Potential hazards to the embryo, fetus, or neonate are numerous and depend on several variables, including the specific virus involved, gestational timing of infection, and whether the infection is primary or recurrent in nature. This article reviews the epidemiology and clinical manifestations of maternal, fetal, and neonatal herpesvirus infections, methods for establishing an accurate etiologic diagnosis, and prevention strategies, including prospects for prenatal diagnosis of these infections.

Adult↗
PubMed1988

Toxoplasmosis: maternal and pediatric findings in 23,000 pregnancies.

An analysis of the antibody titers to toxoplasmosis for 22,845 pregnant women in the Collaborative Perinatal Project was conducted in relation to clinical and laboratory findings in the mothers and children through 7 years of age. More than 900 observations were considered for each mother and child. The major findings were in the children and included a predicted doubling in the frequency of deafness among children born to women with antibody to toxoplasmosis, a predicted 60% increase in microcephaly, and a 30% increase in low IQ (less than 70) in association with the presence of high maternal antibody titer (256 to 512) to toxoplasma. A serologically defined high-risk group of mothers was identified on the basis of high indirect hemagglutination antibody levels or seroconversions and increased IgM toxoplasma antibody levels (indirect fluorescent antibody greater than or equal to 32, enzyme-linked immunosorbent assay greater than or equal to 0.7). Of the 15 pregnancies in this group, two children had congenital toxoplasmosis and three were stillborn.

Antibodies↗
PubMed1988

Perinatal infections and immunity.

An increasing number of infectious agents are now recognized to be important causes of perinatal morbidity and mortality. Most of these agents produce asymptomatic or mild infections in the mother; however, some can cause severe or fatal disease in the fetus. In each case, the infectious agent is transmitted from the mother to the child, usually by the transplacental, hematogenous route. The time of maternal infection during gestation frequently influences the chance of fetal infection and severity of fetal disease. The pathogenesis of these infections involves direct infection of the developing fetal tissues. In some cases this infection can interfere with morphogenesis or cause severe tissue destruction. Very late effects are now recognized with some perinatal infection, thus it is important to conduct longitudinal studies of infected children. Fetal disease can be prevented or reduced if prior exposure of the mother has resulted in complete or partial immunity. Immune responses in the fetus, which become detectable at about 20 to 22 weeks gestation, can be used for diagnostic purposes. They also appear to provide some degree of protection of the fetus from severe or fatal disease with certain agents when infection occurs late in gestation. The prevention of fetal damage by perinatal infections can be accomplished by protection of the mother through the appropriate use of vaccines, avoidance of exposure, treatment with immunoglobulins or the use of chemotherapy. Treatment of the child also involves the use of immunoglobulins and chemotherapy.

Female↗