scholarly journals Ribavirin Protects Syrian Hamsters against Lethal Hantavirus Pulmonary Syndrome — After Intranasal Exposure to Andes Virus

Viruses ◽  
2013 ◽  
Vol 5 (11) ◽  
pp. 2704-2720 ◽  
Author(s):  
Monica Ogg ◽  
Colleen Jonsson ◽  
Jeremy Camp ◽  
Jay Hooper
2018 ◽  
Vol 5 (suppl_1) ◽  
pp. S455-S455
Author(s):  
David Bergamo ◽  
Alfred Bacon ◽  
David Cohen ◽  
Paula Eggers ◽  
Aaron Kofman ◽  
...  

2013 ◽  
Vol 88 (2) ◽  
pp. 811-819 ◽  
Author(s):  
R. L. Brocato ◽  
C. D. Hammerbeck ◽  
T. M. Bell ◽  
J. B. Wells ◽  
L. A. Queen ◽  
...  

2003 ◽  
Vol 77 (18) ◽  
pp. 9894-9905 ◽  
Author(s):  
D. M. Custer ◽  
E. Thompson ◽  
C. S. Schmaljohn ◽  
T. G. Ksiazek ◽  
J. W. Hooper

ABSTRACT Hantavirus pulmonary syndrome (HPS) is a rapidly progressing human disease with one of the highest case fatality rates (30 to 50%) of any acute viral disease known. There are no vaccines, effective antiviral drugs, or immunologics to prevent or treat HPS. In an attempt to develop HPS medical countermeasures, we constructed an expression plasmid, pWRG/AND-M, that contains the full-length M genome segment of Andes virus (ANDV), a South American hantavirus. Transfection experiments in cell culture indicated that both the G1 and G2 glycoproteins are expressed from pWRG/AND-M. Rhesus macaques vaccinated by gene gun with pWRG/AND-M developed remarkably high levels of neutralizing antibodies that not only neutralized ANDV but also cross-neutralized other HPS-associated hantaviruses, including Sin Nombre virus. To determine if the antibodies elicited in the monkeys could confer protection, we performed a series of passive-transfer experiments using a recently described lethal HPS animal model (i.e., adult Syrian hamsters develop HPS and die within 10 to 15 days after challenge with ANDV). When injected into hamsters 1 day before challenge, sera from the vaccinated monkeys either provided sterile protection or delayed the onset of HPS and death. When injected on day 4 or 5 after challenge, the monkey sera protected 100% of the hamsters from lethal disease. These data provide a proof of concept for a gene-based HPS vaccine and also demonstrate the potential value of a postexposure immunoprophylactic to treat individuals after exposure, or potential exposure, to these highly lethal hantaviruses.


2016 ◽  
Vol 132 ◽  
pp. 66-69 ◽  
Author(s):  
Brian H. Bird ◽  
Punya Shrivastava-Ranjan ◽  
Kimberly A. Dodd ◽  
Bobbie R. Erickson ◽  
Christina F. Spiropoulou

2002 ◽  
Vol 66 (6) ◽  
pp. 713-720 ◽  
Author(s):  
M Gonzalez Della Valle ◽  
J Cortez ◽  
A Edelstein ◽  
M L Cacace ◽  
S Miguel ◽  
...  

2020 ◽  
Vol 26 (4) ◽  
pp. 756-759 ◽  
Author(s):  
Daniel O. Alonso ◽  
Unai Pérez-Sautu ◽  
Carla M. Bellomo ◽  
Karla Prieto ◽  
Ayelén Iglesias ◽  
...  

Virology ◽  
1998 ◽  
Vol 241 (2) ◽  
pp. 323-330 ◽  
Author(s):  
P.J. Padula ◽  
A. Edelstein ◽  
S.D.L. Miguel ◽  
N.M. López ◽  
C.M. Rossi ◽  
...  

2007 ◽  
Vol 81 (14) ◽  
pp. 7449-7462 ◽  
Author(s):  
Victoria Wahl-Jensen ◽  
Jennifer Chapman ◽  
Ludmila Asher ◽  
Robert Fisher ◽  
Michael Zimmerman ◽  
...  

ABSTRACT Andes virus (ANDV) and Sin Nombre virus (SNV) are rodent-borne hantaviruses that cause a highly lethal hemorrhagic fever in humans known as hantavirus pulmonary syndrome (HPS). There are no vaccines or specific drugs to prevent or treat HPS, and the pathogenesis is not understood. Syrian hamsters infected with ANDV, but not SNV, develop a highly lethal disease that closely resembles HPS in humans. Here, we performed a temporal pathogenesis study comparing ANDV and SNV infections in hamsters. SNV was nonpathogenic and viremia was not detected despite the fact that all animals were infected. ANDV was uniformly lethal with a mean time to death of 11 days. The first pathology detected was lymphocyte apoptosis starting on day 4. Animals were viremic and viral antigen was first observed in multiple organs by days 6 and 8, respectively. Levels of infectious virus in the blood increased 4 to 5 logs between days 6 and 8. Pulmonary edema was first detected ultrastructurally on day 6. Ultrastructural analysis of lung tissues revealed the presence of large inclusion bodies and substantial numbers of vacuoles within infected endothelial cells. Paraendothelial gaps were not observed, suggesting that fluid leakage was transcellular and directly attributable to infecting virus. Taken together, these data imply that HPS treatment strategies aimed at preventing virus replication and dissemination will have the greatest probability of success if administered before the viremic phase; however, because vascular leakage is associated with infected endothelial cells, a therapeutic strategy targeting viral replication might be effective even at later times (e.g., after disease onset).


2011 ◽  
Vol 7 (12) ◽  
pp. e1002426 ◽  
Author(s):  
David Safronetz ◽  
Marko Zivcec ◽  
Rachel LaCasse ◽  
Friederike Feldmann ◽  
Rebecca Rosenke ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document