Choclo Virus Infection in the Syrian Golden Hamster

Eyzaguirre, Eduardo; Milazzo, Mary Louise; Koster, Frederick; Fulhorst, Charles F.

doi:10.4269/ajtmh.2008.78.669

Cited by 19 publications

(24 citation statements)

References 30 publications

(45 reference statements)

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“…In contrast, levels of antigen appear to be higher in Syrian golden hamsters infected with the human-pathogenic Andes, Maporal (MAPV), or Choclo (CHOV) hantaviruses (11,18,25), although only ANDV and MAPV are pathogenic in hamsters. SNV causes an apathogenic infection in hamsters and elicits a strong neutralizing antibody response by 28 dpi (18); thus, it may be informative to examine the kinetics of neutralizing antibodies in this model.…”

Section: Discussionmentioning

confidence: 91%

Kinetics of Immune Responses in Deer Mice Experimentally Infected with Sin Nombre Virus

Schountz

Acuña-Retamar

Feinstein

et al. 2012

J Virol

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Deer mice are the principal reservoir hosts of Sin Nombre virus, the etiologic agent of most hantavirus cardiopulmonary syndrome cases in North America. Infection of deer mice results in persistence without conspicuous pathology, and most, if not all, infected mice remain infected for life, with periods of viral shedding. The kinetics of viral load, histopathology, virus distribution, and immune gene expression in deer mice were examined. Viral antigen was detected as early as 5 days postinfection and peaked on day 15 in the lungs, hearts, kidneys, and livers. Viral RNA levels varied substantially but peaked on day 15 in the lungs and heart, and antinucleocapsid IgG antibodies appeared in some animals on day 10, but a strong neutralizing antibody response failed to develop during the 20-day experiment. No clinical signs of disease were observed in any of the infected deer mice. Most genes were repressed on day 2, suggesting a typical early downregulation of gene expression often observed in viral infections. Several chemokine and cytokine genes were elevated, and markers of a T cell response occurred but then declined days later. Splenic transforming growth factor beta (TGF-β) expression was elevated early in infection, declined, and then was elevated again late in infection. Together, these data suggest that a subtle immune response that fails to clear the virus occurs in deer mice.

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Section: Discussionmentioning

confidence: 91%

Kinetics of Immune Responses in Deer Mice Experimentally Infected with Sin Nombre Virus

Schountz

Acuña-Retamar

Feinstein

et al. 2012

J Virol

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“…27 However, in hamsters infected with Choclo virus, robust viral replication in the lung is not accompanied by pulmonary inflammation or mortality. 28 Examination of the molecular specificity of this viral protein-integrin interaction may provide clues to the ameliorated pathogenesis in most Choclo virus infections.…”

Section: Discussionmentioning

confidence: 99%

Hantavirus Fever without Pulmonary Syndrome in Panama

Armién¹,

Pascale²,

Muñoz³

et al. 2013

The American Society of Tropical Medicine and Hygiene

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Abstract. In Panama, hantavirus pulmonary syndrome (HPS) is caused by Choclo virus, a species phylogenetically related to Andes and Maporal viruses. Up to 60% of the population has been positive for specific serum antibody in community-based surveys, but mortality is very uncommon. In four western Panama clinics, we tested individuals presenting with a severe febrile prodrome for acute hantavirus (HV) infection by immunoglobulin M enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction as well as clinically similar infections, such as dengue and leptospirosis. From 2006 to 2009, at least 21% of 117 patients diagnosed with HV infection had HV Fever (HF) with no evidence of pulmonary edema (no respiratory distress or radiographic lung infiltrates), and 44% of patients had very mild HPS (radiographic pulmonary edema but no respiratory insufficiency). HV infection caused by Choclo virus in Panama presents often as HF, which contrasts with HV in the Americas but is consistent with the high seroprevalence in endemic regions.

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“…The endothelium in small blood vessels, in particular – pulmonary capillaries, is the primary target of infection in fatal HPS cases (Zaki et al, 1995) and in hamsters infected with ANDV, CHOV, MAPV, or SNV (Eyzaguirre et al, 2008; Hooper et al, 2001; Milazzo et al, 2002; Safronetz et al, 2013). The results of the immunohistochemistry assay in this study suggest that the endothelium in capillaries is the primary target of infection in the lungs of hamsters infected with HTN-007.…”

Section: Discussionmentioning

confidence: 99%

Pneumonitis in Syrian golden hamsters (Mesocricetus auratus) infected with Rio Mamoré virus (family Bunyaviridae, genus Hantavirus)

2014

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Rio Mamoré virus is an etiological agent of hantavirus pulmonary syndrome in South America. The purpose of this study was to determine whether Rio Mamoré virus strain HTN-007 in Syrian golden hamsters is pathogenic. None of 37 adult hamsters infected by intramuscular injection of HTN-007, including 10 animals killed on Day 42 or 43 post-inoculation, exhibited any symptom of disease. Histological abnormalities included severe or moderately severe pneumonitis in 6 (46.2%) of the 13 animals killed on Day 7 or 10 post-inoculation. The primary target of infection in lung was the endothelium of the microvasculature. Collectively, these results indicate that Rio Mamoré virus strain HTN-007 in adult Syrian golden hamsters can cause a nonlethal disease that is pathologically similar to hantavirus pulmonary syndrome.

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Choclo Virus Infection in the Syrian Golden Hamster

Cited by 19 publications

References 30 publications

Kinetics of Immune Responses in Deer Mice Experimentally Infected with Sin Nombre Virus

Kinetics of Immune Responses in Deer Mice Experimentally Infected with Sin Nombre Virus

Hantavirus Fever without Pulmonary Syndrome in Panama

Pneumonitis in Syrian golden hamsters (Mesocricetus auratus) infected with Rio Mamoré virus (family Bunyaviridae, genus Hantavirus)

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