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Biomedical subjects

E Tabor

Publications and source records attributed to E Tabor.

At least 91 records · Page 5Linked to original sources
PubMed1986

Replacement of the deletion in the genome (0.762-0.789 mu) of avirulent HSV-1 HFEM using cloned MluI DNA fragment (0.7615-0.796 mu) of virulent HSV-1 F leads to generation of virulent intratypic recombinant.

The HFEM strain of HSV-1 is apathogenic for the tree shrew by the intraperitoneal (i.p.) route because of a deletion in the genome coordinates 0.762-0.789. Insertion of the MluI DNA fragment (coordinates 0.7615-0.789) cloned from HSV-1 strain F, which is pathogenic for the tree shrew, restored the i.p. pathogenicity to strain HFEM. The recombinant designated R-M1-C1 was highly pathogenic for the tree shrew, but slightly virulent for inbred mouse strain A. It thus appears that the viral DNA sequence involved in the i.p. pathogenicity of HSV-1 is located within the genome coordinates 0.761-0.796. This sequence is recognized differently by the cellular elements involved in HSV-1 infection in the tree shrew and the mouse.

Animals↗
PubMed1985

Horizontal transmission of hepatitis B virus among children and adults in five rural villages in Zambia.

To determine whether horizontal transmission of the hepatitis B virus contributes to the high prevalence of infection with this virus in an endemic region, residents of five villages in Zambia were tested for hepatitis B serologic markers. The prevalence of hepatitis B was determined by testing samples from 620 residents. By examining paired serum samples from 79 children and 80 adults, it was determined that new infections occurred during the five years of this study in at least 14 children (18%) (aged 4-17 years) and ten adults (12%) (aged 23-65 years). These 24 new infections were distributed among 20 households and were not associated with active HBV infections in the mother or, in most cases, other family members. Intervention to prevent hepatitis B in regions such as rural Zambia will require vaccination of susceptible children and adults as well as newborn infants.

Adolescent↗
PubMed1985

Demonstration of a transient rheumatoid factor in the acute phase of hepatitis non A, non B.

The evaluation of an enzyme-linked immunosorbent assay (ELISA) test designed to detect antigens of hepatitis non A, non B (HNANB) revealed that a rheumatoid factor (RF)-like reaction was interfering. This RF-like reaction was not detectable by routine screening methods for RF, such as latex agglutination or the Waaler Rose test. Testing of sequential sera of chimpanzees with acute HNANB showed that this RF-like reaction was present in the acute phase of HNANB simultaneously with alanine aminotransferase (ALT) elevations. Characterization of this RF-like reaction revealed the presence of an IgM antibody against human IgG that banded in CsCl at 1.3 g/ml and at 19S in sucrose gradients. Absorption with IgG-coated latex particles and anti-human IgM gave further evidence of an RF. By testing sera of patients with different forms of acute viral hepatitis, it was demonstrated that an RF-like factor was also present in seven sera from 9 patients with acute hepatitis A, in two sera from 11 patients with hepatitis B, and seven sera from 11 patients with acute HNANB. The rise of RF in the acute phase of hepatitis A may be an effect of polyclonal stimulation of IgM producing B lymphocytes. The high prevalence of RF in HNANB remains unclear as no polyclonal stimulation of IgM has been observed.

Alanine Transaminase↗
PubMed1985

Neutralization of hepatitis B virus infectivity by a murine monoclonal antibody: an experimental study in the chimpanzee.

Two study chimpanzees were inoculated intravenously with approximately 1,000 chimpanzee infectious doses of hepatitis B virus (HBV), one with subtype adr and one with subtype ayw, each previously incubated with 0.1 ml of a murine monoclonal antibody (IgG 1(K) class) directed against a single epitope on hepatitis B surface antigen common to most or all HBV. Two control chimpanzees received identical doses of HBV not incubated with the murine anti-HBs. Neither study chimpanzee developed HBV infection during 12 months of follow-up as judged by normal serum aminotransferase activity, normal liver biopsies, and negative serological tests for HBV-associated antigens and antibodies. In contrast, both control chimpanzees became infected by HBV as evidenced by elevated serum aminotransferase activity, liver biopsy changes characteristic of viral hepatitis, and the appearance of hepatitis B surface antigen (HBsAg) in their sera. Both study chimpanzees were shown to be fully susceptible to infection with these same HBV inocula when challenged 15 months after the initial inoculations at a time when passively administered anti-HBs was no longer detectable. Prior to challenge with HBV, one of the two study chimpanzees received a second injection of the same volume of the murine monoclonal anti-HBs. The survival of this anti-HBs in serum was reduced from six weeks (after the initial injection) to approximately two weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Protection against hepatitis B virus infection by immunization with hepatitis B core antigen.

Although antibody to the hepatitis B surface antigen usually provides protection against hepatitis B virus (HBV) infection, recent reports indicate that this is not always the case. To study the possible role of immune responses to hepatitis B core antigen in immunity to HBV infection, chimpanzees were immunized with chimpanzee liver-derived or genetically cloned hepatitis B core antigen and later challenged with known infectious HBV. Two chimpanzees, which received liver-derived or cloned hepatitis B core antigen in Freund's adjuvant and developed hepatitis B core antibody and low-titer hepatitis B e antibody, were completely protected against HBV infection following challenge. In contrast, another chimpanzee, which received liver-derived hepatitis B core antigen without adjuvant, developed hepatitis B core antibody only in serum and had a subclinical HBV infection when challenged. These findings demonstrate that protection against HBV infection can be induced by immunization with hepatitis B core antigen in adjuvant and that protection, in this case, is not solely dependent on hepatitis B surface antibody. This fact has important implications in our understanding of the biology of HBV infection and in the design of future hepatitis B vaccines.

Animals↗
PubMed1985

Cells from patients with ataxia telangiectasia are abnormally sensitive to the cytotoxic effect of a tumor promoter, phorbol-12-myristate-13-acetate.

Fibroblast strains from 6 patients with ataxia telangiectasia (A-T) were found to be markedly hypersensitive to the cytotoxic action of the tumor promoter phorbol-12-myristate-13-acetate (PMA), their D37 values being 5 times lower than those of two normal controls. Two A-T heterozygous strains were slightly hypersensitive to PMA, while a third one showed normal sensitivity. It is concluded that the DNA lesion which is critical in A-T cells is an important component of the damage caused by PMA-induced free radicals and may play a role both in the tumor-promoting activity of PMA and the cancer proneness of A-T patients.

Ataxia Telangiectasia↗
PubMed1985

In vitro phenotype of ataxia-telangiectasia (AT) fibroblast strains: clues to the nature of the "AT DNA lesion" and the molecular defect in AT.

Studies of the in vitro phenotype of a series of AT strains established in Israel revealed the following features: premature senescence and increased demands for growth factors, normal sensitivity to the cytotoxic effect of alkylating agents, hypersensitivity to agents that damage the deoxyribose moiety of DNA via a "targeted" free radical attack (this hypersensitivity is coupled with reduced inhibition of DNA synthesis compared to normal cells), varying degrees of intermediate hypersensitivity to the same agents in AT heterozygous cells, lack of potentially lethal damage repair and sublethal damage repair in AT homozygous cells following treatment with free radical-producing agents. We conclude that AT involves a DNA repair defect and that the AT DNA lesion is probably a gap with the 3'-phosphate or 3'-phosphoglycolate end left in the DNA following sugar destruction.

Alkylating Agents↗
PubMed1985

Ultrastructural and cytochemical study of hepatocytes and lymphocytes during experimental non-A, non-B infections in chimpanzees.

A human agent of non-A, non-B hepatitis (Inoculum I) was transmitted to chimpanzees and alterations in liver and lymphocytes were studied by electron microscopy and by cytochemical techniques during the acute phase of the disease. Three types of cytoplasmic alterations, consisting of a membraneous and an amorphous part were observed in the hepatocytes. The density of the amorphous constituent decreased after treatment with pronase, but not after treatment with ribonuclease (RNase) or deoxyribonuclease (DNase). The wall of C-III, but not C-II had fibrils with a periodicity the contrast of which markedly increased after pronase treatment. Cytochemical data suggest that the inclusions (C-I-III) represent a cellular reaction to the infectious agent rather than the virus itself. Intranuclear vermicular inclusions (INI) were observed in hepatocytes and lymphocytes as well, mainly in degenerating cells. Tubuloreticular inclusions (TRS) did not appear in circulating lymphocytes during acute infection; however, they could be induced by human alpha interferon treatment in vitro. Increased numbers of lymphocytes with parallel tubular arrays (PTA) were noted at the peak of serum aminotransferase elevations. The latter two alterations (TRS and PTA) most likely represent immunologic reactions of the host to the infectious agent.

Animals↗
PubMed1984

Community-acquired non-A, non-B hepatitis: clinical characteristics and chronicity.

The characteristics of 86 patients with acute non-A, non-B hepatitis were compared to 23 patients with acute hepatitis A and 76 with acute hepatitis B by medical record reviews of patients seen at 5 hospitals in Baltimore, Maryland, as part of case-control study of viral hepatitis. Results of serum aminotransferase levels, bilirubin, albumin, and prothrombin times alone could not distinguish the type of viral hepatitis because of extensive overlap. The alanine aminotransferase range for non-A, non-B hepatitis was 56 to 1819 IU/liters, for hepatitis A 250 to 1995 IU/liters, and for hepatitis B 203 to 2120 IU/liters. The ranges of aspartate aminotransferase and bilirubin for the types of hepatitis also overlapped. Fewer patients with non-A, non-B hepatitis or hepatitis A had a prolonged prothrombin time compared to patients with hepatitis B. Hepatic encephalopathy was seen only in two patients with hepatitis B. Forty-two percent of non-A, non-B hepatitis patients followed for 6 months or longer continued to have elevated alanine aminotransferase levels. Chronic alanine aminotransferase elevation was independent of the source of infection: transfusion, parenteral drug use, or all other sources. Prolonged follow-up is necessary to evaluate chronicity in patients with non-A, non-B hepatitis.

Alanine Transaminase↗
PubMed1984

Ultrastructural alterations in serial liver biopsy specimens from chimpanzees experimentally infected with a human non-A, non-B hepatitis agent.

Four chimpanzees experimentally infected with an agent of human non-A, non-B hepatitis were studied to determine the sequence of ultrastructural alterations in hepatocytes during infection. Three of the four types of cytoplasmic alterations previously described in association with non-A, non-B hepatitis were observed in the hepatocytes. Sponge-like cytoplasmic inclusions (designated C-I) were detected at or near the time of peak serum aminotransferase elevations in two of the four chimpanzees. Undulating membranes (designated C-II) were observed in all four chimpanzees, at the time of the first elevation of serum aminotransferase levels. Cytoplasmic tubules (designated C-III) were first observed four, eight, and twelve weeks, respectively, after inoculation in three of the chimpanzees. Four weeks after the peak of serum aminotransferase elevations, cytoplasmic alterations could no longer be detected in hepatocytes of the four chimpanzees. Intranuclear inclusions consisting of 20-27 nm granules and vermicular particles were observed in hepatocytes from preinoculation liver biopsy specimens, as well as biopsies obtained during non-A, non-B hepatitis. The number of these particles was greatest near the time of peak elevation of serum aminotransferase levels, however. Tubulo-crystalline inclusions were noted as well in the endothelial cells from both preinoculated and infected chimpanzees. Cytoplasmic alterations in hepatocytes of chimpanzees experimentally infected with an agent of non-A, non-B hepatitis appear characteristic of infection with this agent. In contrast, intranuclear particles were not specifically related to the non-A, non-B hepatitis infection.

Animals↗