Induction and Suppression of Innate Antiviral Responses by Hepatitis A Virus

Newcastle disease (ND) has been a consistent risk factor to the poultry industry worldwide. Its pathogen, Newcastle disease virus (NDV), is also a promising antitumor treatment candidate. The pathogenic mechanism has intrigued the great curiosity of researchers, and advances in the last two decades have been summarized in this paper. The NDV’s pathogenic ability is highly related to the basic protein structure of the virus, which is described in the Introduction of this review. The overall clinical signs and recent findings pertaining to NDV-related lymph tissue damage are then described. Given the involvement of cytokines in the overall virulence of NDV, cytokines, particularly IL6 and IFN expressed during infection, are reviewed. On the other hand, the host also has its way of antagonizing the virus, which starts with the detection of the pathogen. Thus, advances in NDV’s physiological cell mechanism and the subsequent IFN response, autophagy, and apoptosis are summarized to provide a whole picture of the NDV infection process.

Section: Receptors For Ndv Pampmentioning

confidence: 99%

Pathologic Mechanisms of the Newcastle Disease Virus

Zhang

Ding

2023

“…This is evidenced by the fact that MAVS, a central protein in IFN pathway signalling, is also targeted at the RNA and protein levels via different mechanisms by FMDV VP1, L pro and 3A [ 44 , 57 , 58 ]. Many other viruses have made MAVS one of the key points in the fight against the antiviral response, including picornaviruses such as HRV-1A, hepatitis A virus (HAV) and SVV, which target MAVS via the 2A and 3C; 2B and precursor 3ABC; and 3C proteins, respectively [ 66 , 67 , 68 ]. Similarly, NEMO, the protein responsible for the formation of the IKK complex, is also impacted by FMDV 3C, responsible for its swine form cleavage, at the Gln383 residue, to prevent NF-kB activation [ 49 , 59 , 69 ].…”

Section: Discussionmentioning

confidence: 99%

Host-Specific Interplay between Foot-and-Mouth Disease Virus 3D Polymerase and the Type-I Interferon Pathway

Sarry

Caignard

Dupré

et al. 2023

Foot-and-mouth disease (FMD) is a highly contagious viral disease affecting cloven-hoofed animals. One of the issues related to this disease is the persistence of its causative agent, foot-and-mouth disease virus (FMDV). While the mechanisms of FMDV persistence remain unclear, there are clues that it may be related to protein–protein interactions (PPI) between viral proteins and cellular proteins involved in the interferon (IFN) response. Since FMDV persistence has been described in cattle, sheep and goats but not in swine, we screened PPI involving FMDV proteins and sixteen major type-I IFN pathway proteins from these four species by nanoluciferase-2-hybrid complementation assay, in order to identify new PPI and determine their host specificity. As the results concerning the 3Dpol were the most interesting in view of the limited data concerning its role in immune escape, we decided to focus particularly on this protein. The identified PPI were confirmed by GST pull-down. We identified PPI between 3Dpol and seven IFN pathway proteins, namely, IKKα, IKKε, IRF3, IRF7, NEMO, MDA5 and MAVS. These PPI are conserved among the four studied species, with the exception of the one between 3Dpol and MAVS, which was only found with the swine protein. We also showed, using luciferase reporter assays, that 3Dpol could inhibit the induction phase of the IFN pathway. These results demonstrate, for the first time, a putative role for 3Dpol in FMDV innate immune escape.

“…In the light of the current literature, some picornaviruses seem to focus more on these last two targets rather than on MDA5. This is notably the case of HRV-1A, which targets MAVS via 2A and 3C, hepatitis A virus (HAV), which also targets MAVS via 2B, and precursor 3ABC [ 205 , 206 ]. This is also the case for SVV, which blocks the action of RIG-I via 2C and 3C, a protein also capable of cleaving MAVS and other proteins situated further downstream of the IFN pathway [ 121 , 207 , 208 ].…”

Section: Discussion and Concluding Remarksmentioning

confidence: 99%

Foot-and-Mouth Disease Virus: Molecular Interplays with IFN Response and the Importance of the Model

Sarry

Vitour

Zientara

et al. 2022

Foot-and-mouth disease (FMD) is a highly contagious viral disease of cloven-hoofed animals with a significant socioeconomic impact. One of the issues related to this disease is the ability of its etiological agent, foot-and-mouth disease virus (FMDV), to persist in the organism of its hosts via underlying mechanisms that remain to be elucidated. The establishment of a virus–host equilibrium via protein–protein interactions could contribute to explaining these phenomena. FMDV has indeed developed numerous strategies to evade the immune response, especially the type I interferon response. Viral proteins target this innate antiviral response at different levels, ranging from blocking the detection of viral RNAs to inhibiting the expression of ISGs. The large diversity of impacts of these interactions must be considered in the light of the in vitro models that have been used to demonstrate them, some being sometimes far from biological systems. In this review, we have therefore listed the interactions between FMDV and the interferon response as exhaustively as possible, focusing on both their biological effect and the study models used.