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M Asanaka

Publications and source records attributed to M Asanaka.

9 recordsLinked to original sources
PubMed1997

Human carcinoembryonic antigen and biliary glycoprotein can serve as mouse hepatitis virus receptors.

Receptors for murine coronavirus mouse hepatitis virus (MHV) are members of the murine carcinoembryonic antigen (CEA) gene family. Since MHV can also infect primates and cause central nervous system lesions (G. F. Cabirac et al., Microb. Pathog. 16:349-357, 1994; R. S. Murray et al., Virology 188:274-284, 1992), we examined whether human CEA-related molecules can be used by MHV as potential receptors. Transfection of plasmids expressing human carcinoembryonic antigen (hCEA) and human biliary glycoprotein into COS-7 cells, which lack a functional MHV receptor, conferred susceptibility to two MHV strains, A59 and MHV-2. Domain exchange experiments between human and murine CEA-related molecules identified the immunoglobulin-like loop I of hCEA as the region conferring the virus-binding specificity. This finding expands the potential MHV receptors to primate species.

Amino Acid Sequence↗
PubMed1995

A pregnancy-specific glycoprotein is expressed in the brain and serves as a receptor for mouse hepatitis virus.

Mouse hepatitis virus (MHV), a murine coronavirus known to cause encephalitis and demyelination, uses murine homologues of carcinoembryonic antigens as receptors. However, the expression of these receptors is extremely low in the brain. By low-stringency screening of a mouse brain cDNA library, we have identified a member of the pregnancy-specific glycoprotein (PSG) subgroup of the carcinoembryonic antigen gene family. Unlike other PSG that are expressed in the placenta, it is expressed predominantly in the brain. Transfection of the cDNA into COS-7 cells, which lack a functional MHV receptor, conferred susceptibility to infection by some MHV strains, including A59, MHV-2, and MHV-3, but not JHM. Thus, this is a virus strain-specific receptor. The detection of multiple receptors for MHV suggests the flexibility of this virus in receptor utilization. The identification of this virus in receptor utilization. The identification of a PSG predominantly expressed in the brain also expands the potential functions of these molecules.

Amino Acid Sequence↗
PubMed1995

Neuropathogenicity of mouse hepatitis virus JHM isolates differing in hemagglutinin-esterase protein expression.

The hemagglutinin-esterase (HE) protein of mouse hepatitis virus (MHV) is an optional envelope protein present in only some MHV isolates. Its expression is regulated by the copy number of a UCUAA pentanucleotide sequence present in the leader sequence of the viral genomic RNA. The functional significance of this viral protein so far is not clear. In this report, we compared the neuropathogenicity of two MHV isolates, JHM(2) and JHM(3), which express different amounts of HE protein. Intracerebral inoculation of these two viruses into C57BL/6 mice showed that JHM(2), which expresses an abundant amount of HE protein, was more neurovirulent than JHM(3), which expresses very little HE. Histopathology showed that early in infection, JHM(2) infected primarily neurons, while JHM(3) infected mainly glial cells. JHM(3) eventually infected neurons and caused a delayed death relative to JHM(2)-infected mice, suggesting that the progression of JHM(3) infection in the central nervous system was slower than JHM(2). In vitro infection of JHM(3) in primary mixed glial cell cultures of astrocyte-enriched cultures yielded higher virus titers than JHM(2), mimicking the preferential growth of JHM(3) in glial cells in vivo. These findings suggest that the reduced neuropathogenicity of JHM(3) may correlate with its preferential growth in glial cells. Sequence analysis showed that the S genes of these two viruses are identical, thus ruling out the S gene as the cause of the difference in neuropathogenicity between these two viruses. We conclude that the HE protein contributes to viral neuropathogenicity by influencing either the rate of virus spread, viral cell tropism or both.

Acetylesterase↗
PubMed1993

A spike protein-dependent cellular factor other than the viral receptor is required for mouse hepatitis virus entry.

Previous studies have shown that some mouse strains are resistant to mouse hepatitis virus (MHV) infection despite the presence of functional viral receptors (K. Yokomori and M. M. C. Lai, J. Virol. 66, 6931-6938, 1992). To determine the molecular requirement for MHV infection, several cell lines derived from both susceptible and resistant mouse strains were tested for their ability to support infection by two different MHV strains, JHM and A59. Most of the cell lines tested, including ones from susceptible mouse strains, exhibited selective resistance to JHM, but were susceptible to A59, suggesting that there is an additional cellular factor(s) discriminating JHM from A59 infection. Both RNA and protein syntheses of JHM were inhibited in the resistant cells; however, transfection of JHM genomic RNA into these cells led to the production of infectious virus, suggesting that the restriction step(s) is during an early stage of viral replication cycle. The mRNA for the MHV receptor (the murine homolog of the carcinoembryonic antigen) is expressed in all cell lines, and expression in COS cells of the receptor isolated from the resistant murine cell lines rendered the COS cells susceptible to both A59 and JHM infections. Furthermore, the transfection of additional MHV receptors into the resistant cells did not overcome the resistance to JHM virus infection. These results suggested that the viral receptor is functional; nevertheless, the JHM infection is restricted at an early step of infection in these cells. The study of the growth properties of the various recombinant viruses between A59 and JHM revealed that one of the viral genes determining viral replication in these cell lines is the S protein gene; thus, the second factor required for viral infection may interact directly or indirectly with the S protein at an early step of infection. Taken together, these studies suggest that expression of a functional viral receptor is not sufficient to establish MHV infection, and that an additional factor(s) is required for an early step of viral infection, possibly during virus entry.

Animals↗
PubMed1993

Cell fusion studies identified multiple cellular factors involved in mouse hepatitis virus entry.

We have previously reported that certain murine cell lines are susceptible to mouse hepatitis virus (MHV) A59 strain infection but resistant to JHM strain, despite the expression of the viral receptor for both strains. This restriction on viral infection has been shown to occur at the virus entry level (Yokomori et al., Virology 196, 45-56, 1993). To study whether JHM resistance of these cell lines is due to a defective cellular factor necessary for JHM virus entry, or due to the presence of an inhibitor, hybrid cells were obtained by polyethylene glycol (PEG)-mediated fusion between two resistant cell lines, i.e., a Balb/c mouse-derived cell line, BC10 cells, which are resistant to JHM infection but express a viral receptor, and the simian cell line COS cells, which are resistant to JHM because of the absence of the viral receptor. JHM could replicate in the hybrid BC10-COS cells, indicating that the restriction of viral infection in BC10 cells could be complemented by COS cells. This result indicates that the resistance of BC10 cells to JHM infection is due to the defectiveness of a cellular factor rather than the presence of an inhibitor. JHM virus-binding and penetration into BC10 cells appeared to be normal. However, JHM internalization into BC10 cells by PEG-induced virus-cell fusion did not lead to viral replication, suggesting that the restriction of JHM infection in BC10 cells is at the level of viral uncoating. This restriction could be complemented by PEG-mediated fusion with other murine cell lines which have the virion-uncoating activity, but not by cell lines which lack this activity. Furthermore, the viral resistance of most of other murine cell lines, which express MHV receptors, could not be overcome by fusion with COS cells, suggesting that different murine cell lines are defective in different viral entry functions. Therefore, we conclude that JHM viral entry process requires multiple cellular factors secondary to the viral receptor.

Adsorption↗
PubMed1990

Budding process and maturation of human immunodeficiency virus examined by means of pre- and post-embedding immunocolloidal gold electron microscopy.

The techniques of pre- and post-embedding immunocolloidal gold electron microscopy were tested for their usefulness for analyzing the morphogenesis of human immunodeficiency virus (HIV) strain LAV employing U-937 cells persistently infected with the virus (U-937/LAV). By both techniques the following results were obtained. (1) Budding process was restricted to a localized area at the membrane adjacent to the Golgi apparatus. (2) The distribution of viral envelope antigens was restricted to the electron-dense crescent structures on the cell surface. (3) Virions released from the cells could be classified mainly into 2 categories: virions with doughnut-shaped cores or with conical cores at the center of the particles. And p24 proteins localized on the thick electron-dense cores of both types. These findings support the idea that pre- and post-embedding immunogold electron microscopy is very useful for studying the morphogenesis of viruses.

HIV↗
PubMed1988

An improved method for the detection of HIV antigen in the blood of carriers.

The measurement of HIV antigen levels in sera or plasma of HIV-infected individuals is critical for determining the existence of antigen or infectious virus before seroconversion and for prognosis. Pretreatment of sera or plasma of HIV carriers by heating at 70 degrees C for 10 min at an acidic pH enabled us to estimate antigens efficiently in immune complexes. This procedure will also be useful in determining antigen levels in HIV carriers more precisely.

Acquired Immunodeficiency Syndrome↗
PubMed1988

[AIDS and human lymphocytes].

HIV infection is no doubt the primary cause of AIDS. But the relationship between HIV and its host lymphocytes is fairly complicated. It has become clear that the host range of the viruses varies according to the clinical stage of the patients from whom viruses were isolated. Besides, the cause or mechanism of cell killing by HIV infection is not well-known. The density of CD4 molecules on the cell surface can not simply explain the phenomena, such as the level of virus growth, killing mechanisms of lymphocytes and host range of the virus. It is quite interesting to analyse which gene of the virus determines the characteristics of the virus.

Acquired Immunodeficiency Syndrome↗