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Biomedical subjects

A Aranda-Anzaldo

Publications and source records attributed to A Aranda-Anzaldo.

12 recordsLinked to original sources
PubMed1992

Human immunodeficiency virus type 1 productive infection in staurosporine-blocked quiescent cells.

Staurosporine, an antibiotic known to inhibit cellular protein kinases, can reversibly block the progress of normal and tumour cells into the cell cycle. The ability of HIV-1 to infect and replicate in cells blocked by staurosporine was investigated. The results show that blocked, non-cycling cells can be productively infected by HIV-1, steadily releasing infectious progeny virus for several weeks. This suggests that at least in some cases, HIV-1 can be found in a stable and active state in resting, non-proliferating T cells.

Alkaloids↗
PubMed1992

Altered chromatin higher-order structure in cells infected by herpes simplex virus type 1.

In cells infected by herpesviruses chromosomal aberrations such as breaks and constrictions are commonly observed. Previous studies have shown that chromatin modifications in cells infected by herpes simplex virus type 1 (HSV-1) are not due to extensive breakdown of host-cell DNA or disruption of nucleosomal structure. We have previously shown that infection by HSV-1 induces single-stranded breaks in the host-cell DNA in a time-dependent fashion. Here we report that the early DNA damage observed in virus-infected cells is related to modifications in the higher-order structure of host-cell chromatin. Such modifications seem to be of a more permanent nature than the DNA single-stranded breaks.

Chromatin↗
PubMed1992

Early induction of DNA single-stranded breaks in cells infected by herpes simplex virus type 1.

In cells infected with herpesviruses a series of host-cell nuclear changes can be observed in a temporal sequence, such changes include chromosome aberrations. The precise mechanism by which virus infection produces chromosome damage is not known. Previous studies have revealed modifications in the properties of chromatin from infected cells, but such modifications are not due to extensive breakdown of host DNA or alteration of the nucleosomal structure in bulk host chromatin. We have adapted and modified a fluorescence enhancement assay for DNA damage in order to study the effects of herpes simplex virus type 1 infection on the integrity of the host-cell DNA. Here it is reported that HSV-1 induces a significant number of single-stranded breaks in the host-cell DNA at early hours post-infection. Such breaks seem not to be directly related to the major breakdown of host-cell DNA seen at later times post-infection.

Animals↗
PubMed1992

Chemical inactivation of human immunodeficiency virus in vitro.

Most chemicals with potential virucidal activity are extremely cytotoxic even at very small concentrations, thus introducing a number of technical problems and uncertainties in the evaluation of the net virucidal effect. In the present study, an attempt was made to confirm the reported virucidal activity of certain well-known chemicals and a number of new compounds were investigated. The results suggest that HIV inactivation is dependent on the viral concentration, the time of incubation in presence of the putative disinfectant and the degree of virucidal activity of the latter. The data illustrate methodological problems arising from residual cytotoxicity of the chemical which may mask or mimic the presence of a true virucidal activity and lead to erroneous conclusions. Alcohol, the most commonly used disinfectant, was found to be ineffective for high viral concentrations, whilst sodium hypochlorite was the most efficient.

Antiviral Agents↗
PubMed1992

HHV-6 inhibition by two polar compounds.

Dimethyl sulphoxide and dimethyl formamide, two polar compounds and powerful cell differentiation inducers, inhibit HHV-6 infection when added to HHV-6-infected HSB2 cultures. This was established by a delay in the time-course of infection and in the development of virus-induced cytopathic effects. Furthermore, viral titration of supernatants showed a significant reduction (3 log10) of the number of infectious particles. Electron microscopy confirmed that viable cells and extracellular virions were present in the cultures containing the polar compounds, while in the non-treated cultures all cells were lysed and no extracellular virus was evident. The mode of action of these compounds is still unclear and warrants further investigation.

Antiviral Agents↗
PubMed1992

Possible cell-free prion replication.

Spongiform encephalopathies, such as scrapie or bovine spongiform encephalopathy in animals, or kuru, Creutzfeld-Jakob disease (CJD) and Gerstmann-Sträussler-Scheinker disease (GSS) in man, seem to be caused by a transmissible agent whose nature is still a matter of debate. The properties of this agent which has been designated as prion, differ from those of any other known infectious agents, including viruses and viroids. Several lines of evidence suggest that the prion is devoid of nucleic acid and is identical with a modified form of a normal host protein. This lack of nucleic acid poses the question of how a protein moiety can propagate itself as a transmissible agent. Here it is proposed that prion replication is a process similar to crystallization and as such, the propagation of prions can take place as a sort of chain-reaction in an in vitro cell-free system.

Animals↗
PubMed1992

Evidence for an altered kinetics of DNA excision-repair in cells infected by herpes simplex virus type 1.

In cells infected with herpesviruses a series of host cell nuclear changes can be observed in a temporal sequence. Such changes include chromosome aberrations. The precise mechanism by which virus infection produces chromosome damage is not known, but we have previously reported that herpes simplex virus type 1 (HSV-1) induces a significant number of single-stranded breaks in the host cell DNA at early hours of infection and in a time-dependent fashion. Here, it is reported that HSV-1-infected cells subjected to irradiation with ultraviolet light, show an altered kinetics in the normal process of DNA excision-repair at early hours of infection.

Animals↗
PubMed1991

On the regulation of DNA methylation by higher-order structure in the cell nucleus.

Several years ago it was postulated that DNA methylation may play a role in the regulation of gene activity in animal cells. Progress has been made in establishing the mechanisms by which methylation influences gene expression, but little is known about the mechanisms that control methylation itself. Here is proposed a model, susceptible of experimental confirmation, which suggests that chromatin higher-order structure is a determinant factor for the regulation of DNA methylation. The background for such a model as well as current evidence in support of it are discussed.

Animals↗
PubMed1991

A role for CD8+ T lymphocytes in the pathogenesis of AIDS.

Experimental and clinical evidence is presented which supports the hypothesis that CD8+ T lymphocytes aimed at suppressing HIV replication in infected CD4+ T cells may have an important role in the pathogenesis of AIDS by directly causing a decrease in CD4+ T lymphocyte numbers. Possible models to test this hypothesis are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Dimethyl sulfoxide inhibits human immunodeficiency virus production in vitro.

LDV/7, H9, and MOLT-4, three cell lines infectible by human immunodeficiency virus were incubated with dimethyl sulfoxide, an inducer of cell differentiation. It was shown that this is a powerful inhibitor of viral production, but its effect is transient: viral production resumes when the compound is removed from the culture medium. It does not inactivate the virus, and it fails to prevent viral infection or to inhibit expression of p24 on the surface of the infected cells.

Cell Line↗
PubMed1990

Is immune oversuppression the direct cause of AIDS?

AIDS is presumably caused by HIV, a retrovirus. The main support for this view comes from the consistent epidemiological correlation between AIDS and the presence of antibody against HIV. Several HIV-associated mechanisms have been described to explain the cytopathic effects on helper-T-lymphocytes observed in vitro but so far, none of these mechanisms has been confirmed in vivo. On the other hand, there is virtually no free virus and HIV RNA synthesis is very low both in AIDS patients and in asymptomatic carriers. Thus it is unlikely that HIV causes AIDS by acting as a conventional cytocidal virus. Here it is proposed, on the basis of current experimental evidence, that an active immune suppression mediated by T8+ cells is the direct culprit for a gradual decline of helper-T-lymphocyte numbers leading to an immunocompromised state in AIDS. The role of HIV in triggering and perpetuating a state of immune oversuppression is discussed.

Acquired Immunodeficiency Syndrome↗