Viral interference between low pathogenic avian influenza H9N2 and avian infectious bronchitis viruses in vitro and in ovo

Aouini, Rim; Laamiri, Nacira; Ghram, Abdeljelil

doi:10.1016/j.jviromet.2018.06.011

Cited by 16 publications

(12 citation statements)

References 42 publications

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“…while other co-infection groups had conditional effects on the proliferation of PPRV and GTPV. This suggested that the two viruses competitively proliferate when inoculated on GSF cells, which was quite different from the results of other studies on viral interference [ 36 ]. Other studies found that under co-infection with PCV2 and Gram-negative bacteria, AIV, and NDV, the replication of only one virus was reduced [ 37 , 38 ].…”

Section: Discussioncontrasting

confidence: 94%

In vitro and in vivo analyses of co-infections with peste des petits ruminants and capripox vaccine strains

Zhang

Yang

Zhang

et al. 2021

Virol J

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Background Peste des petits ruminants (PPR) and goat pox (GTP) are two devastating animal epidemic diseases that affect small ruminants. Vaccination is one of the most important measures to prevent and control these two severe infectious diseases. Methods In this study, we vaccinated sheep with PPR and POX vaccines to compare the changes in the antibody levels between animals vaccinated with PPRV and POX vaccines alone and those co-infected with both vaccines simultaneously. The cell infection model was used to explore the interference mechanism between the vaccines in vitro. The antibody levels were detected with the commercial ELISA kit. The Real-time Quantitative PCR fluorescent quantitative PCR method was employed to detect the viral load changes and cytokines expression after the infection. Results The concurrent immunization of GTP and PPR vaccine enhanced the PPR vaccine's immune effect but inhibited the immune effect of the GTP vaccine. After the infection, GTP and PPR vaccine strains caused cytopathic effect; co-infection with GTP and PPR vaccine strains inhibited the replication of PPR vaccine strains; co-infection with GTP and PPR vaccine strains enhanced the replication of GTP vaccine strains. Moreover, virus mixed infection enhanced the mRNA expressions of TNF-α, IL-1β, IL-6, IL-10, IFN-α, and IFN-β by 2–170 times. GTP vaccine strains infection alone can enhanced the mRNA expression of IL-1β, TNF-α, IL-6, IL-10, while the expression of IFN-α mRNA is inhibited. PPR vaccine strains alone can enhanced the mRNA expression of IFN-α, IFN-β, TNF-α, and has little effect the mRNA expression of IL-1β, IL-6 and IL-10. The results showed that GTP and PPR vaccine used simultaneously in sheep enhanced the PPR vaccine's immune effect but inhibited the immune effect of the GTP vaccine in vivo. Furthermore, an infection of GTP and PPR vaccine strains caused significant cell lesions in vitro; co-infection with GTP + PPR vaccine strains inhibited the replication of PPR vaccine strains, while the co-infection of GTP followed by PPR infection enhanced the replication of GTP vaccine strains. Moreover, virus infection enhanced the expressions of TNF-α, IL-1β, IL-6, IL-10, IFN-α, and IFN-β. Conclusions Peste des petits ruminants and capripox vaccine strains interfere with each other in vivo and vitro.

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Section: Discussioncontrasting

confidence: 94%

In vitro and in vivo analyses of co-infections with peste des petits ruminants and capripox vaccine strains

Zhang

Yang

Zhang

et al. 2021

Virol J

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“…H9N2 is important due to its widespread circulation in domestic poultry, especially in the presence of other co-infecting pathogens. For example, co-infection with E. coli and H9N2 could cause more serious synergistic pathogenic effects, indicating the role of both pathogens as complicating factors in poultry infections [12,13].…”

Section: Introductionmentioning

confidence: 99%

Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Chu¹,

Guo²,

Zhang³

et al. 2020

Preprint

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Simple Summary: Chlamydia psittaci, an obligate intracellular gram-negative bacterium and economically relevant pathogen in poultry and pet birds, could cause psittacosis/ornithosis, and is also a human pathogen causing atypical pneumonia after zoonotic transmission. H9N2 influenza virus, a low pathogenic avian influenza viruses subtype, has become endemic in different types of domestic poultry in lots of countries, resulting in great economic loss due to reduced egg production or high mortality associated with co-infection with other pathogens. These two pathogens are easily mixed with other pathogens to aggravate the disease, and C. psittaci and H9N2 often cause mixed infection. Co-infection of C. psittaci with H9N2 commonly induces severe pneumonia and high mortality in SPF chickens. According to previous studies, we postulated that C. psittaci infection may beneficial for the replication of H9N2 in HD11. Consequently, in this study, we clarify the pathogenic mechanism of coinfection with C. psittaci and H9N2 in the chicken macrophage cell line HD11, which is the first study of the coinfection of C. psittaci and H9N2 in vitro. Abstract:We investigated the effect regarding coinfection of C. psittaci and H9N2 on HD11 cells, expecting to find the potential pathogenesis of the coinfection induced airsacculitis. HD11 cells were infected with C. psittaci and/or H9N2 in different orders, and effects of the coinfection on iNOS expression and activity, NO synthesis, cell phagocytosis, and cytokines in HD11 cells were determined. Results showed that coinfection of C. psittaci and H9N2 significantly aggravated the mortality of HD11 cells compared to one pathogen alone. Furthermore, C. psittaci infection increased the replication of H9N2 in HD11 cells, whereas decreased the iNOS, enzyme activity, and NO of HD11 cells with H9N2 infection. Additionally, H9N2 also increased the pathogen loads of C. psittaci in HD11 cells. We also found that C. psittaci infection alone significantly decreased the phagocytosis of HD11 cells, compared to H9N2 alone. What's more, C. psittaci infection increased type Th2 cytokines IL-6 and IL-10 of HD11 cells with H9N2 infection. All the above data indicated that primary C. psittaci infection is able to aggravate H9N2 invasion by down-regulating functions of HD11 cells.Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 12 March 2020

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“…Previous studies on in vitro and in ovo interference between AIV and IBV-H120 using, respectively, cultured chicken embryo lung cells and embryonated SPF eggs, have shown that the second inoculated virus slows down the process of viral replication of the first administered one [36]. At the same age, groups simultaneously infected had numerically lower antibody titers as compared to groups singly or sequentially infected.…”

Section: Discussionmentioning

confidence: 93%

Viral interference between H9N2-low pathogenic avian influenza virus and avian infectious bronchitis virus vaccine strain H120 in vivo

Aouini

Laamiri

Nsiri

et al. 2019

Comparative Immunology, Microbiology and Infectious Diseases

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Viral interference between low pathogenic avian influenza H9N2 and avian infectious bronchitis viruses in vitro and in ovo

Cited by 16 publications

References 42 publications

In vitro and in vivo analyses of co-infections with peste des petits ruminants and capripox vaccine strains

In vitro and in vivo analyses of co-infections with peste des petits ruminants and capripox vaccine strains

Primary Infection of Chlamydia psittaci Triggers Invasion of H9N2 Avian Influenza Virus by Impairing Functions of Chicken Macrophages

Viral interference between H9N2-low pathogenic avian influenza virus and avian infectious bronchitis virus vaccine strain H120 in vivo

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