A Rapid Method for Detecting Junin Virus Viremia in the Guinea Pig

Intervirology ◽  
1977 ◽  
Vol 8 (6) ◽  
pp. 360-363 ◽  
Author(s):  
Adriana Rabinovich ◽  
Patricio M. Cossio ◽  
Guadalupe Carballal ◽  
Roberto M. Arana
1985 ◽  
Vol 15 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Lucía B. de Guerrero ◽  
Martha C. Boxaca ◽  
Ester Malumbres ◽  
María de las Mercedes Gómez

1987 ◽  
Vol 23 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Cristina B. Dejean ◽  
Bethy L. Ayerra ◽  
Angélica R. Teyssié

Intervirology ◽  
1983 ◽  
Vol 19 (1) ◽  
pp. 44-46 ◽  
Author(s):  
Fernando N. Dulout ◽  
Guadalupe Carballal ◽  
Néstor O. Bianchi ◽  
Huberto N. von Guradze

Intervirology ◽  
1985 ◽  
Vol 24 (4) ◽  
pp. 193-198 ◽  
Author(s):  
Fernando N. Dulout ◽  
Horacio E. Panisse ◽  
Guadalupe Carballal ◽  
Huberto N. von Guradze ◽  
Julio C. DeLuca ◽  
...  

Intervirology ◽  
1985 ◽  
Vol 23 (4) ◽  
pp. 190-198 ◽  
Author(s):  
Martha C. Boxaca ◽  
María de las Mercedes Gómez ◽  
Ester Malumbres ◽  
Lucía B. deGuerrero

2015 ◽  
Vol 89 (11) ◽  
pp. 5949-5956 ◽  
Author(s):  
Alexey V. Seregin ◽  
Nadezhda E. Yun ◽  
Milagros Miller ◽  
Judith Aronson ◽  
Jennifer K. Smith ◽  
...  

ABSTRACTThe New World arenavirus Junin virus (JUNV) is the causative agent of Argentine hemorrhagic fever (AHF), a potentially deadly disease endemic to central regions of Argentina. The live-attenuated Candid #1 (Can) strain of JUNV is currently used to vaccinate the human population at risk. However, the mechanism of attenuation of this strain is still largely unknown. Therefore, the identification and functional characterization of viral genetic determinants dictating JUNV virulence or attenuation would significantly improve the understanding of the mechanisms underlying AHF and facilitate the development of novel, more effective, and safer vaccines. Here, we utilized a reverse genetics approach to generate recombinant JUNV (rJUNV) strains encoding different gene combinations of the pathogenic Romero (Rom) and attenuated Can strains of JUNV. All strains of rJUNV exhibitedin vitrogrowth kinetics similar to those of their parental counterparts. Analysis of virulence of the rJUNV in a guinea pig model of lethal infection that closely reproduces the features of AHF identified the envelope glycoproteins (GPs) as the major determinants of pathogenesis and attenuation of JUNV. Accordingly, rJUNV strains expressing the full-length GPs of Rom and Can exhibited virulent and attenuated phenotypes, respectively, in guinea pigs. Mutation F427I in the transmembrane region of JUNV envelope glycoprotein GP2 has been shown to attenuate the neurovirulence of JUNV in suckling mice. We document that in the guinea pig model of AHF, mutation F427I in GP2 is also highly attenuating but insufficient to prevent virus dissemination and development of mild clinical and pathological symptoms, indicating that complete attenuation of JUNV requires additional mutations present in Can glycoprotein precursor (GPC).IMPORTANCEDevelopment of antiviral strategies against viral hemorrhagic fevers, including AHF, is one of the top priorities within the Implementation Plan of the U.S. Department of Health and Human Services Public Health Emergency Medical Countermeasures Enterprise. Live-attenuated Candid #1 strain, derived from the 44th mouse brain passage of the prototype XJ strain of JUNV, has been demonstrated to be safe, immunogenic, and highly protective and is currently licensed for human use in Argentina. However, the bases for the attenuated phenotype of Candid #1 have not been established. Therefore, the identification and functional characterization of viral genetic factors implicated in JUNV pathogenesis and attenuation would significantly improve the understanding of the molecular mechanisms underlying AHF and facilitate the development of novel antiviral strategies.


2013 ◽  
Vol 7 (12) ◽  
pp. e2614 ◽  
Author(s):  
Brian B. Gowen ◽  
Terry L. Juelich ◽  
Eric J. Sefing ◽  
Trevor Brasel ◽  
Jennifer K. Smith ◽  
...  

1988 ◽  
Vol 24 (1) ◽  
pp. 97-99 ◽  
Author(s):  
C. B. Dejean ◽  
J. R. Oubiña ◽  
G. Carballal ◽  
A. R. Teyssié

1983 ◽  
Vol 12 (4) ◽  
pp. 273-280 ◽  
Author(s):  
Mercedes C. Weissenbacher ◽  
Marta S. Sabattini ◽  
María M. Avila ◽  
Patricia M. Sangiorgio ◽  
María R. F. De Sensi ◽  
...  

2011 ◽  
Vol 55 (10) ◽  
pp. 4631-4638 ◽  
Author(s):  
Benjamin W. Neuman ◽  
Lydia H. Bederka ◽  
David A. Stein ◽  
Joey P. C. Ting ◽  
Hong M. Moulton ◽  
...  

ABSTRACTMembers of theArenaviridaefamily are a threat to public health and can cause meningitis and hemorrhagic fever, and yet treatment options remain limited by a lack of effective antivirals. In this study, we found that peptide-conjugated phosphorodiamidate morpholino oligomers (PPMO) complementary to viral genomic RNA were effective in reducing arenavirus replication in cell cultures andin vivo. PPMO complementary to the Junín virus genome were designed to interfere with viral RNA synthesis or translation or both. However, only PPMO designed to potentially interfere with translation were effective in reducing virus replication. PPMO complementary to sequences that are highly conserved across the arenaviruses and located at the 5′ termini of both genomic segments were effective against Junín virus, Tacaribe virus, Pichinde virus, and lymphocytic choriomeningitis virus (LCMV)-infected cell cultures and suppressed viral titers in the livers of LCMV-infected mice. These results suggest that arenavirus 5′ genomic termini represent promising targets for pan-arenavirus antiviral therapeutic development.


Sign in / Sign up

Export Citation Format

Share Document