Biomedical subjects

M Krivjanská

Publications and source records attributed to M Krivjanská.

8 recordsLinked to original sources

PubMed1996

The syn3 strain HSZP of herpes simplex virus type 1 (HSV-1) is not pathogenic for mice and shows limited neural spread.

Strain HSZP of the herpes simplex virus type 1 (HSV-1) forms large giant cells in vitro. This property was found associated with a mutation that alters the codon CGC (in the strain KOS or 17 sequence) to CAC (in the HSZP sequence), changing the amino acid 857 from arginine to histidine in the cytoplasmic domain of the glycoprotein B (gB) polypeptide chain. Giant cell formation by ANGpath was attributed to a mutation that alters the codon GCC (in KOS and strain 17 sequences) to GTC (in ANGpath sequence) changing the amino acid 854 in the same (syn3) region of the gB molecule. In contrast to the ANGpath virus, which is pathogenic (1 LD50 < 1 x 10(4) PFU) for adult DBA/2 mice after peripheral inoculation, strain HSZP was never found to be lethal for adult mice. Whereas ANGpath-infected mice which survived acute infection frequently (79%) developed latency in the regional sensory ganglion (as proved by virus reactivation during explantation), latent HSZP reactivated in ganglion culture at a considerably reduced rate (21%). Only 10-day-old DBA/2 mice were sensitive to HSZP infection. In these, HSZP spread from the site of peripheral administration mainly by hematogenous route. The neural spread of HSZP in suckling DBA/2 mice was manifested by the involvement of vegetative neurons in the wall of the small intestine and in the retroperitoneal vegetative ganglia. We conclude that HSZP, a polykaryocyte-forming strain with a mutation in the syn3 region II, shows limited neuroinvasity for mice after peripheral administration.

Animals↗

PubMed1994

Specific binding of herpes simplex virus type 1 (HSV-1) strain HSZP to host cell surface can provoke interference with early shutoff of host protein synthesis induced by HSV-1 strain KOS.

The HSZP strain of herpes simplex virus type 1 (HSV-1) is defective with respect to the early shutoff of host protein synthesis but is effective at interfering with the early shutoff function of the HSV-1 KOS strain, even when heat-inactivated or neutralized by antibody. The interference was not due to exclusion of strain KOS by HSZP at the level of adsorption or penetration. The component responsible for the interference is an integral part of HSZP virions. Strain HSZP inactivated with zinc ions failed to interfere with the early shutoff function of the superinfecting strain KOS. The same effect was also found with strain HSZP purified from cells treated with 2-deoxy-D-glucose. This finding supports the idea that a specific interaction between HSZP virions and the cell surface can be responsible for the interference phenomenon.

Animals↗

PubMed1992

Herpes simplex virus type 1 (HSV-1) HSZP interferes also after antibody neutralization with early shutoff of host protein synthesis induced by HSV-1 KOS.

The HSZP strain of herpes simplex virus type 1 (HSV-1) is defective with respect to the early shutoff of host protein synthesis. However, in superinfection experiments using Vero cells, the HSZP strain was effective, even after neutralization by antibody, at interfering with the early shutoff function of the HSV-1 KOS strain. Evidence was given that the observed interference was not due to exclusion of the KOS by HSZP at the level of adsorption or penetration. The neutralized KOS strain failed to induce early shutoff of host protein synthesis.

Animals↗

PubMed1991

The synthesis of the major DNA-binding protein (ICP8) in cells infected with the strain HSZP or KOS of herpes simplex virus type 1.

Synthesis of the major DNA-binding protein (ICP8) was investigated in primary rabbit kidney (RK) and Vero cells infected with the syncytial (syn) strain HSZP or with the non-syn strain KOS of herpes simplex virus type 1 (HSV-1). Results showed the following: 1. In contrast to strain KOS, the rate of viral polypeptide synthesis was accelerated in Vero cells infected with strain HSZP. The ICP8 could be detected in the nuclei of cells by one hour post-infection (hr p. i.) where it became associated with the viral DNA (DNase sensitive form). Later on (7 hr p.i.), the synthesis of viral polypeptides decreased and no further translocation of ICP8 from the cytoplasm into the nucleus was observed. 2. Strain HSZP was approx. three times more resistant to the action of phosphonoacetic acid (PAA) than strain KOS. In order to block the synthesis of HSZP gamma-2 polypeptides, a concentration of 600 micrograms PAA/ml had to be used. Under this condition, the HSZP ICP8 was translocated into the cell nucleus at later interval only (7 hr p.i.), and it was still possible to release this polypeptide from the nucleus by DNase treatment. The failure of the HSZP ICP8 to associate with the nuclear matrix (DNase resistant form) of infected cells in the absence of viral DNA replication may reflect its predominant affinity for the viral DNA which, in turn, may be responsible for the observed accelerated synthesis of the HSZP polypeptides in infected Vero cells. 3. In primary RK cells infected with strain HSZP the ICP8 did not translocate into the cell nucleus. Therefore, no gamma-2 polypeptides were synthesized.

Animals↗

PubMed1991

Immunoprecipitation of herpes simplex virus polypeptides with human sera is related to their ELISA titre.

Out of 485 human sera tested by neutralization and enzyme immunoassay 13 were negative in both tests, while a positive correlation was found in 457 samples (94.3%). The rest of sera (3.2%) showed discordant results. Selected sera were examined, in addition, by Western blot and immunoprecipitation assays with the aim to analyse the precipitation profile of discordant sera and correlate the ELISA titre with the precipitation profiles. High titre sera precipitated the main glycoproteins (gC, gB, gE, gD), the capsid polypeptides (VP 5, VP 19, VP 21, VP 22) and several other structural and nonstructural proteins. The ability of sera to precipitate viral structural proteins was related to their ELISA titre rather than to their neutralizing activity.

Adult↗

PubMed1989

Mechanism of altered cytoskeleton organization in influenza virus infection.

We followed the autophosphorylation of cytoskeleton (CS) isolated from control chick embryo cell membranes (CS-C) and from these membranes after influenza virus adsorption (CS-V) under conditions allowing to determine the activity of a single type proteinkinase. The Ca2+ dependent calmodulin (CaM) kinase used different substrates from CS-V than did the c'AMP dependent proteinkinase. The catalytic subunit (c-subunit) of the c'AMP dependent proteinkinase added from outside phosphorylated the same polypeptides than the endogenous c'AMP dependent proteinkinase, the further being more active than the latter. The purified influenza virus incorporated 32P in the presence of the c-subunit only. Incubation of influenza virus with the c-subunit caused morphological changes visible by electron microscopy. The pleomorphy of the particles as well as their electron transmissibility were enhanced in result of structural alterations and rarefaction of surface spikes of the haemagglutinin and neuraminidase. The contractibility of CS isolated from normal CEC and of the CS from CEC by 15 min postinfection (p.i.) was determined according to the actomyosin ATPase activity. The ATPase activity of the cytoskeleton in the presence of the Ca2+/CaM and that in the presence of c'AMP were used as controls. The virus as well as the Ca2+/CaM increased the ATPase activity. EGTA had no effect but did not interfere with virus stimulation, while c'AMP blocked the virus-induced enhancement of the ATPase activity.

Actins↗

PubMed1988

Herpes simplex virus type 1 (HSV-1) HSZP interferes also heat inactivated with early shutoff of host protein synthesis induced by HSV-1 KOS.

The ability of two strains of herpes simplex virus type 1 (HSZP and KOS) to shut off the host protein synthesis in the presence of Actinomycin D was investigated. The HSZP strain proved to be defective with respect to the so-called early shutoff function. In superinfection experiments, the HSZP was effective at interfering with the early shutoff function of the KOS strain provided that the HSZP infection preceded KOS superinfection. Heat inactivation of the HSZP did not lead to the loss of its interfering ability. Evidence was given that this interference was neither due to the hindrance of the KOS by HSZP at adsorption nor due its exclusion during penetration.

Animals↗

PubMed1978

Marked difference in electrophoretic migration rates between two influenza A viruses.

Comparative moving boundary electrophoresis revealed that influenza virus A/PR/8/34 (H0N1) has a 2.5 times higher electrophoretic migration rate at pH 7 than influenza virus A/Singpore/1/57 (H2N2). This difference was the same whether the compared viruses were purified first by either ammonium sulphate precipitation or adsorption onto and elution from red blood cells and then by density gradient centrifugation. The same electrophoretic methods was used for testing the homogeneity of influenza virus preparations purified by either method.

Centrifugation, Density Gradient↗