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Am. J. Trop. Med. Hyg., 74(3), 2006, pp. 449-456
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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SEROTYPE-SPECIFIC DIFFERENCES IN CLINICAL MANIFESTATIONS OF DENGUE

ANGEL BALMASEDA, SAMANTHA N. HAMMOND, LEONEL PÉREZ, YOLANDA TELLEZ, SAIRA INDIRA SABORÍO, JUAN CARLOS MERCADO, RICARDO CUADRA, JULIO ROCHA, MARIA ANGELES PÉREZ, SHEYLA SILVA, CRISANTA ROCHA, AND EVA HARRIS*
Departamento de Virología, Centro Nacional de Diagnóstico y Referencia, Ministerio de Salud, Managua, Nicaragua; Division of Infectious Diseases, School of Public Health, University of California, Berkeley, California; Hospital Escuela Oscar Danilo Rosales Arguello, León, Nicaragua; Infectious Diseases Unit, Hospital Infantil Manuel de Jesús Rivera, Managua, Nicaragua

Dengue, the most prevalent arthropod-borne viral disease of humans, is caused by four serotypes of dengue virus (DENV 1–4). Although all four DENV serotypes cause a range of illness, defining precisely which clinical characteristics are associated with the distinct serotypes has been elusive. A cross-sectional study was conducted on 984 and 313 hospitalized children with confirmed DENV infections during two time periods, respectively, in the same hospitals in Nicaragua: a 3-year period (1999–2001) when DENV-2 accounted for 96% of the viruses identified, and the 2003 dengue season when DENV-1 predominated (87% of identified serotypes). When the two periods were compared, more shock (OR 1.91, 95% CI 1.35–2.71) and internal hemorrhage (OR 2.05, CI 1.16–3.78) were observed in the period when DENV-2 predominated, whereas increased vascular permeability was associated to a greater degree with the DENV-1 period (OR 2.36, CI 1.80–3.09). Compared with the DENV-2 period, the DENV-1 season was associated with more hospitalized primary dengue cases (OR 3.86, CI 2.72–5.48) and more primary DENV infections with severe manifestations (OR 2.93, CI 2.00–4.28). These findings provide new data to characterize the pathogenic potential of distinct DENV serotypes in human populations.


Received May 4, 2005. Accepted for publication November 11, 2005.

Acknowledgments: We would like to thank Nidia Soza, Soraya Solano, Wendy Idiaquez, Sonia Arguello, Yoryelin Rodriguez, Iskra Valenzuela, Ninoska Robles, Luisa Amanda Campo, Juan José Amador, and Alcides Gonzalez, without whom this study could not have been performed. We are grateful to Stephen Waterman for editorial review.

Financial support: This work was supported by grant TW-0095 from the Fogarty International Center (NIH) and grant 2002 HE-098 from the Rockefeller Foundation to E.H, as well as grant 1CA4-CT-2001-10086 from the European Union.

* Address correspondence to Eva Harris, Division of Infectious Diseases, School of Public Health, 140 Warren Hall, University of California, Berkeley, CA 94720-7360, Telephone: 510-642-4845, Fax: 510-642-6350. E-mail: eharris{at}berkeley.edu

Authors’ addresses: Angel Balmaseda, Leonel Pérez, Yolanda Tellez, Saira Indira Saborío, and Juan Carlos Mercado, Departamento de Virologia, Centro Nacional de Diagnóstico y Referencia, Ministerio de Salud, Complejo de Salud Dra. Concepcion Palacios, Primero de Mayo, Managua, Nicaragua, Telephone/Fax: 011-505-289-7723. Samantha Nadia Hammond and Eva Harris, Division of Infectious Diseases, School of Public Health, 140 Warren Hall, University of California, Berkeley, CA 94720-7360, Telephone: 510-642-4845, Fax: 510-642-6350. Ricardo Cuadro and Julio Rocha, Hospital Escuela Dr. Oscar Danilo Rosales Arguello (HEODRA), de la Iglesia Catedral 1 cuadra al sur, León, Nicaragua, Telephone/Fax: 011 505 311-5939. Maria Angeles Pérez, Sheyla Silva, and Crisanta Rocha, Hospital Infantil Manuel de Jesus Rivera "La Mascota," Barrio Ariel Darce, Distrito no. 5, Managua, Nicaragua, Telephone: 011-505-289-7702, Fax: 011-505-289-7408.

Reprint requests: Eva Harris, Division of Infectious Diseases, School of Public Health, 140 Warren Hall, University of California, Berkeley, CA 94720-7360, Telephone: 510-642-4845, Fax: 510-642-6350, E-mail: eharris{at}berkeley.edu.




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