Abstract
Both influenza A virus (IAV) and influenza D virus (IDV) are enzootic in pigs. IAV causes approximately 100% morbidity with low mortality, whereas IDV leads to only mild respiratory diseases in pigs. In this study, we performed a series of coinfection experiments in vitro and in vivo to understand how IAV and IDV interact and cause pathogenesis during coinfection. The results showed that IAV inhibited IDV replication when infecting swine tracheal epithelial cells (STECs) with IAV 24 or 48 h prior to IDV inoculation and that IDV suppressed IAV replication when IDV preceded IAV inoculation by 48 h. Virus interference was not identified during simultaneous IAV/IDV infections or with 6 h between the two viral infections, regardless of their order. The interference pattern at 24 and 48 h correlated with proinflammatory responses induced by the first infection, which, for IDV, was slower than for IAV by about 24 h. The viruses did not interfere with each other if both infected the cells before proinflammatory responses were induced. Coinfection in pigs further demonstrated that IAV interfered with both viral shedding and virus replication of IDV, especially in the upper respiratory tract. Clinically, coinfection of IDV and IAV did not show significant enhancement of disease pathogenesis, compared with the pigs infected with IAV alone. In summary, this study suggests that interference during coinfection of IAV and IDV is primarily due to the proinflammatory response; therefore, it is dependent on the time between infections and the order of infection. This study facilitates our understanding of virus epidemiology and pathogenesis associated with IAV and IDV coinfection.
Highlights
Influenza viruses are classified into types A, B, C and D according to the genetic and antigenic properties of the nucleoprotein (NP) and matrix 1 (M1) genes [1,2]
To compare the proinflammatory responses stimulated by influenza A virus (IAV) and influenza D virus (IDV), we evaluated both gene and protein expression in swine tracheal epithelial primary cells (STECs) for a set of proinflammatory markers, including type I interferon (IFN-β), type II interferon (IFN-γ), tumor necrosis factor-alpha (TNF-α), DDX58 (retinoic acid-inducible gene I (RIGI)), interleukin (IL)-1β, IL-4, IL-6, IL8, IL-10, IP-10, C–C chemokine ligand 5 (CCL5) and C-X-C
Motif Chemokine Ligand 9 (CXCL9) (Table 1), which were reported in IAV and/or IDV
Summary
Influenza viruses are classified into types A, B, C and D according to the genetic and antigenic properties of the nucleoprotein (NP) and matrix 1 (M1) genes [1,2]. Whereas influenza B and C viruses are documented to infect only humans and swine, influenza. A virus (IAV) and influenza D virus (IDV) can infect a wide range of hosts. A low level of human exposure to IDV is documented [9]. Based upon the surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), IAV is further classified into 18 HA and 11 NA types [11,12]. Different from IAV, IDV encodes a hemagglutinin–esterase-fusion (HEF) surface glycoprotein that catalyzes receptor binding, cleavage and membrane fusion [3,13,14], resembling the functions of HA and NA for IAV
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