Search PubMed⌕ Search

Biomedical subjects

R A Weiss

Publications and source records attributed to R A Weiss.

At least 199 records · Page 11Linked to original sources
PubMed1992

A measles virus isolate from a child with Kawasaki disease: sequence comparison with contemporaneous isolates from 'classical' cases.

We examined the relationship between a measles virus isolate from a child with Kawasaki disease and two contemporaneous wild-type isolates from children with 'classical' measles and the Schwarz vaccine strain. Sequence analysis of 3118 bp from the nucleoprotein, matrix, fusion and haemagglutinin genes of each virus revealed that the isolate from the child with Kawasaki disease was not related to measles vaccine strains and did not contain any of the marked abnormalities previously found in subacute sclerosing panencephalitis isolates, but was more akin to wild-type isolates currently circulating in the U.K. A comparison of our sequences with those obtained from earlier wild-type U.K. isolates suggests significant evolution of measles virus in the U.K. over the last decade.

Amino Acid Sequence↗
PubMed1992

The Bulletin of the North American Society of Phlebology. Insurance Advisory Committee Report.

The treatment of varicose veins as taught within the specialty of phlebology consists of the best combinations of sclerotherapy and surgery after a thorough evaluation by physical examination and Doppler ultrasound, as well as other techniques. Although patients can experience some relief of symptoms by external compression hosiery, only treatment that closes up leaky valves will stop the progression of disease. Sclerotherapy is a safe, well-accepted, non-investigational, highly effective method to treat abnormally enlarged veins. Surgical procedures may be necessary to supplement sclerotherapy in certain anatomic sites. Varicose veins cause patients to experience pain, lose time from work, and can ultimately lead to permanent disability. Our healthcare system must provide the most high quality cost effective care for these patients. By keeping costs down as compared with full-scale surgical procedures, the approach of sclerotherapy or sclerotherapy with outpatient surgery, performed by properly trained physicians, provides a means to accomplish this. Medical necessity criteria allow exclusion of payments for patients seeking treatment purely for cosmetic needs.

Cardiology↗
PubMed1992

Mapping of homologous, amino-terminal neutralizing regions of human T-cell lymphotropic virus type I and II gp46 envelope glycoproteins.

Twelve synthetic peptides containing hydrophilic amino acid sequences of human T-cell lymphotropic virus type I (HTLV-I) envelope glycoprotein were coupled to tetanus toxoid and used to raise epitope-specific antisera in goats and rabbits. Low neutralizing antibody titers (1:10 to 1:20) raised in rabbits to peptides SP-2 (envelope amino acids [aa] 86 to 107), SP-3 (aa 176 to 189), and SP-4A (aa 190 to 209) as well as to combined peptide SP-3/4A (aa 176 to 209) were detected in the vesicular stomatitis virus-HTLV-I pseudotype assay. Higher-titered neutralizing antibody responses to HTLV-I (1:10 to 1:640) were detected with pseudotype and syncytium inhibition assays in four goats immunized with a combined inoculum containing peptides SP-2, SP-3, and SP-4A linked to tetanus toxoid. These neutralizing anti-HTLV-I antibodies were type specific in that they did not inhibit HTLV-II syncytium formation. Neutralizing antibodies in sera from three goats could be absorbed with peptide SP-2 (aa 86 to 107) as well as truncated peptides containing envelope aa 90 to 98, but not with equimolar amounts of peptides lacking envelope aa 90 to 98. To map critical amino acids that contributed to HTLV-I neutralization within aa 88 to 98, peptides in which each amino acid was sequentially replaced by alanine were synthesized. The resulting 11 synthetic peptides with single alanine substitutions were then used to absorb three neutralizing goat antipeptide antisera. Both asparagines at positions 93 and 95 were required for adsorption of neutralizing anti-HTLV-I antibodies from all three sera. Peptide DP-90, containing the homologous region of HTLV-II envelope glycoprotein (aa 82 to 97), elicited antipeptide neutralizing antibodies to HTLV-II in goats that were type specific. In further adsorption experiments, it was determined that amino acid differences between homologous HTLV-I and HTLV-II envelope sequences at HTLV-I aa 95 (N to Q) and 97 (G to L) determined the type specificity of these neutralizing sites. Thus, the amino-terminal regions of HTLV-I and -II gp46 contain homologous, linear, neutralizing determinants that are type specific.

Amino Acid Sequence↗
PubMed1992

Feline leukemia virus subgroup B uses the same cell surface receptor as gibbon ape leukemia virus.

Pseudotypes of gibbon ape leukemia virus/simian sarcoma-associated virus (GALV/SSAV) and feline leukemia virus subgroup B (FeLV-B) have been constructed by rescuing a Moloney murine leukemia virus vector genome with wild-type GALV/SSAV or FeLV-B. The resulting recombinant viruses utilized core and envelope proteins from the wild-type virus and conferred resistance to growth in L-histidinol upon infected cells by virtue of the HisD gene encoded by the vector genome. They displayed the host range specificity of the rescuing viruses and could be neutralized by virus-specific antisera. Receptor cross-interference was observed when the GALV/SSAV or FeLV-B pseudotypes were used to superinfect cells productively infected with either GALV/SSAV or FeLV-B. Although murine cells are resistant to FeLV-B infection, murine cells expressing the human gene for the GALV/SSAV receptor became susceptible to FeLV-B infection. Therefore GALV/SSAV and FeLV-B utilize the same cell surface receptor.

3T3 Cells↗
PubMed1992

Human immunodeficiency virus type 2 infection and fusion of CD4-negative human cell lines: induction and enhancement by soluble CD4.

We describe human immunodeficiency type 2 (HIV-2) strains which induce cell-to-cell fusion and infect certain CD4- human cell lines. Soluble CD4 (sCD4) induces or enhances fusion by most HIV-2 strains tested. Soluble CD4-immunoglobulin G chimeras and conjugates of sCD4 and antibody to the third domain of CD4 block HIV-2 fusion of CD4- cells. We conclude that HIV-2 can enter CD4- cells via an alternative cell surface receptor to CD4. While some strains entered efficiently, others retained a dependency on an interaction with sCD4 to initiate changes in the virion envelope required for membrane fusion.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Retroviruses and human cancer.

Retroviruses have long been associated with cancer in many species. Human T cell leukaemia virus type I causes adult T cell leukaemia. Human immunodeficiency virus infection is associated with lymphoma and Kaposi sarcoma, but oncogenesis is largely secondary to its effect on the immune system. The incidence of Kaposi sarcoma varies greatly in different social groups with AIDS, being most frequent among male homosexuals; an unknown, sexually transmissible agent may be responsible. Human endogenous retroviral genomes are linked with myeloproliferative disease. Finally, the risk is discussed that cancer could be a side-effect of the use of retroviral vectors in human gene therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1991

A murine cell line producing HTLV-I pseudotype virions carrying a selectable marker gene.

A murine cell line, EH, expressing the gag and pol proteins of Moloney murine leukemia virus (Mo-MLV) as well as an Mo-MLV recombinant genome with a selectable marker (histidinol dehydrogenase), was transfected with a plasmid coding for the gene of the human T-cell leukemia virus type I (HTLV-I) envelope precursor (gp62), placed under the control of the human cytomegalovirus immediate early promoter. One clone, T. 14, was recovered, in which gp62 RNA and protein were detected. Supernatant from this clone transferred the HisD gene to a panel of cell lines which express receptors for HTLV-I, but was unable to pass the marker gene to cells which do not express receptors. The colony-forming units were sensitive to HTLV-I receptor interference and to specific neutralization by anti-HTLV-I serum. These data show that hybrid virions were produced in which the envelope proteins of HTLV-I had pseudotyped Mo-MLV capside particles containing a selectable recombinant viral genome.

Animals↗
PubMed1991

HTLV-1 envelope sequences from Brazil, the Caribbean, and Romania: clustering of sequences according to geographic origin and variability in an antibody epitope.

We sequenced the envelope genes of Human T-cell leukemia type I viruses (HTLV-I) derived from five Brazilian, two Caribbean, and one Romanian case of adult T-cell leukemia after amplification of the complete env gene by PCR. A comparison with previously reported HTLV-I sequences revealed that, although highly homologous, no two env sequences were identical. All envelope sequences differed from each other by 0.3-2.1% nucleotide differences. The five Brazilian sequences clustered together and were about as different from each other (0.5-0.75% nucleotide difference) as were three previously reported Japanese sequences (0.7-0.95%). In contrast, sequences of Caribbean origin were less homogeneous (0.5-1.9% nucleotide differences within this group). The Romanian sequence was not significantly more divergent than any of the others and was closest to our two Caribbean sequences. We observed two changes in a region (aa 176-209) which has previously been shown to contain a linear antibody epitope recognized by most human sera from seropositive individuals. One of these changes affects the binding of monoclonal antibodies to this epitope demonstrating the variability of an antibody epitope in the HTLV-I envelope.

Amino Acid Sequence↗
PubMed1991

Rat monoclonal antibodies to nonoverlapping epitopes of human immunodeficiency virus type 1 gp120 block CD4 binding in vitro.

Monoclonal antibodies (MAbs) to a recombinant form of the envelope glycoprotein gp120 of human immunodeficiency virus type 1 (HIV-1 IIIB) were raised in rats and screened for their ability to block recombinant gp120 binding to recombinant, soluble CD4 (sCD4) in vitro. Four such MAbs were identified and characterised. Each MAb bound strongly to gp120 from eight widely divergent HIV-1 strains from the United States and Africa. Two MAbs were mapped to the fourth conserved (C4) region of gp120, whereas the other two recognised an as yet undefined, conformationally sensitive epitope. MAbs to the latter epitope were the more potent in blocking the gp120-sCD4 interaction. None of the MAbs, however, had potent neutralising activity.

Animals↗
PubMed1991

Specific cell surface requirements for the infection of CD4-positive cells by human immunodeficiency virus types 1 and 2 and by Simian immunodeficiency virus.

Human CD4 was expressed on a range of mammalian cell lines. CD4+ non-primate cells, derived from rat, hamster, mink, cat, and rabbit, bind recombinant gp120 of human immunodeficiency virus type 1 (HIV-1) but are resistant to HIV-1 infection. CD4 expression on various human, rhesus, and African green monkey cell lines confers differential susceptibilities for HIV-1, HIV-2, and simian immunodeficiency (SIV) strains. For example, CD4+ TE671 rhabdomyosarcoma cells are sensitive to HIV-1 and HIV-2 but resistant to SIV, whereas CD4+ U87 glioma cells are resistant to HIV-1 infection but sensitive to HIV-2 and SIV. HIV-1 infection was not dependent on human major histocompatibility class I expression. Studies of cell fusion and of infection by vesicular stomatitis virus pseudotypes bearing HIV-1 and HIV-2 envelopes showed that the differential cell tropisms of HIV-1, HIV-2, and SIV are determined at the cell surface.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Recombinant CD4-selected human immunodeficiency virus type 1 variants with reduced gp120 affinity for CD4 and increased cell fusion capacity.

Variants of molecularly cloned human immunodeficiency virus type 1 (HIV-1) were analyzed following selection for the ability to replicate after exposure to soluble, recombinant CD4 protein (rCD4). Two variants, 4/1 and 16/2, show 8-fold and 16-fold reduced sensitivity to rCD4 neutralization yet remain as sensitive as the parental wild-type (wt) virus to neutralization by rCD4-immunoglobulin G (IgG) chimeric molecules and to inhibition of cellular infection by anti-CD4 antibody. The 4/1 variant is more cytopathic, with faster cell fusion and replication kinetics than the wt virus. The gp120s derived from the 4/1 and 16/2 variants have 3-fold and 30-fold reduced binding affinities to rCD4, respectively. The 4/1 variant exhibits diminished shedding of virion gp120 induced by rCD4. The binding of and neutralization by V3 loop antibodies and other anti-gp120 antibodies is reduced for 4/1 but not for 16/2. Sequence analysis revealed a codon change at amino acid residue 435 in the C4 region of the gp120 of 16/2. This accounts for its rCD4 insensitivity, since the insertion of this mutation in the wt gp120 yields the same phenotype. The 4/1 variant has a codon change in the V3 region of gp120 (amino acid 311), which accounts for its reduced sensitivity to some neutralizing antibodies but not to rCD4. The ready selection of rCD4-resistant variants has obvious relevance for rCD4-based therapeutic stratagems.

Amino Acid Sequence↗