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Open AccessJournal ArticleDOI

Viremic dissemination of mouse hepatitis virus-JHM following intranasal inoculation of mice.

Stephen W. Barthold, +1 more
- 01 Jan 1992 - 
- Vol. 122, Iss: 1, pp 35-44
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TLDR
The pattern of mouse hepatitis virus (MHV) JHM dissemination in blood and other tissues was examined during the first 5 days following intranasal inoculation and suggested lymphatic spread of virus to cervical lymph node and mesenteric lymph node as pathways of dissemination in addition to viremia.
Abstract
Using a sensitive infant mouse bioassay to detect infectious virus, the pattern of mouse hepatitis virus (MHV) JHM dissemination in blood and other tissues was examined during the first 5 days following intranasal inoculation. MHV replicated in nasal turbinates of both susceptible BALB and resistant SJL mice from days 1 through 5, but BALB mice had higher titers on days 1 and 2. Viremia was detectable on days 1 through 5 in BALB mice, but only on days 3 and 5 in SJL mice. Transient virus replication occurred in the lungs of both mouse genotypes at 1 and 2 days, then ceased. This correlated with more consistently demonstrable virus in blood collected from the left atrium of the heart, compared to jugular vein, portal vein and right atrial blood. Virus was associated equally with the plasma and cellular fractions of blood on day 3, but was primarily in the buffy coat of the cellular fraction on day 5. Interferon-α/β was detected in serum and spleen, but not liver or brain of BALB mice or in any tissue of SJL mice. BALB serum and spleen interferon was first detected at 36h, peaked between 48 and 72h, and was undetectable by 108h. The distribution of virus in nose, cervical, axillary and mesenteric lymph nodes, spleen, Peyer's patch, thymus, bone marrow and liver was examined at 1, 2, and 3 days. The resulting pattern suggested lymphatic spread of virus to cervical lymph node and mesenteric lymph node as pathways of dissemination in addition to viremia.

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References
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TL;DR: A convenient assay for interferons based on reduction of cytopathic effect was developed and can be used with various types of cells and a variety of viruses.
Book ChapterDOI

The Biology and Pathogenesis of Coronaviruses

TL;DR: The coronavirases were first recognized and morphologically defined as a group by Tyrrell and co-workers (1968, 1975, 1978) and biochemical studies have recently provided additional information which allows better characterization of these agents.
Journal ArticleDOI

Genetic resistance to mouse hepatitis virus correlates with absence of virus-binding activity on target tissues.

TL;DR: SJL/J mice may be resistant to mouse hepatitis virus A59 infection because they lack a specific virus receptor which is present on the plasma membranes of target cells from genetically susceptible BALB/c and semisusceptible C3H mice.
Journal ArticleDOI

Purification of the 110-kilodalton glycoprotein receptor for mouse hepatitis virus (MHV)-A59 from mouse liver and identification of a nonfunctional, homologous protein in MHV-resistant SJL/J mice.

TL;DR: SJL/J mice express a protein which shares some sequence homology with the MHV receptor but which lacks virus-binding activity and is not recognized by the blocking anti-receptor MAb, suggesting resistance of SJL/j mice to MHV-A59 may be due to absence or mutation of the virus- binding domain in the nonfunctional receptor homolog in SJL-susceptible mice.
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Immunopathology of mouse hepatitis virus type 3 infection. Role of humoral and cell-mediated immunity in resistance mechanisms.

TL;DR: In this paper, Humoral and cell-mediated immune responses were studied in resistant and susceptible strains of mice infected with mouse hepatitis virus type III (MHV 3) by regular passages in susceptible DBA/2 mice and assayed by LD-50 determination.
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