Concomitant helminth infection downmodulates the Vaccinia virus-specific immune response and potentiates virus-associated pathology. Issue 1 (January 2017)

• Record Type: Journal Article
• Authors: Gazzinelli-Guimarães, Pedro Henrique; de Freitas, Lorena Falabella Daher; Gazzinelli-Guimarães, Ana Clara; Coelho, Fabiana; Barbosa, Fernando Sérgio; Nogueira, Denise; Amorim, Chiara; Dhom-Lemos, Lucas de Carvalho; Oliveira, Luciana Maria; da Silveira, Alexandre Barcelos; da Fonseca, Flávio Guimarães; Bueno, Lilian Lacerda; Fujiwara, Ricardo Toshio
• Is Part Of: International journal for parasitology. Volume 47:Issue 1(2017)
• Page Start: 1
• Page End: 10
• Publication Date: 2017-01
• Subjects: Larval ascariasis -- Vaccinia virus, co-infection -- Immunomodulation -- Lung inflammation -- Helminth immunology; Parasitology -- Periodicals; Parasitology -- Periodicals; Parasitologie -- Périodiques; Parasitology; Periodicals; Electronic journals; 571.999
• DOI: 10.1016/j.ijpara.2016.08.007
• Languages: English
• ISSNs: 0020-7519

Abstract

Graphical abstract: Highlights: Ascaris sp. and Vaccinia virus (VACV) co-infection aggravates the virus-associated pathology. Ascaris sp. and VACV co-infection enhances virus titres in the lung, leading to a marked increase in mortality. A reduction in CD4 + IFN-γ + T cells is associated with increased morbidity in co-infection. There is a negative association between the coincident larval Ascaris and respiratory VACV infection. Co-infected mice presented a marked decrease in the total number of migrating Ascaris lung-stage larvae. Abstract: The aim of this work was to elucidate the immunopathological mechanisms of how helminths may influence the course of a viral infection, using a murine model. Severe virulence, a relevant increase in the virus titres in the lung and a higher mortality rate were observed in Ascaris and Vaccinia virus (VACV) co-infected mice, compared with VACV mono-infected mice. Immunopathological analysis suggested that the ablation of CD8 + T cells, the marked reduction of circulating CD4 + T cells producing IFN-γ, and the robust pulmonary inflammation were associated with the increase of morbidity/mortality in co-infection and subsequently with the negative impact of concomitant pulmonary ascariasis and respiratory VACV infection for the host. On the other hand, when evaluating the impact of the co-infection on the parasitic burden, co-infected mice presented a marked decrease in the total number of migrating Ascaris lung-stage larvae in comparison with Ascaris mono-infection. Taken together, our major findings suggest that Ascaris and VACV co-infection may potentiate the virus-associated pathology by the downmodulation of the VACV-specific immune response. Moreover, this study provides new evidence of how helminth parasites may influence the course of a coincident viral infection.