Table 2.

Recent findings related to intrinsic molecules and biological processes involved in IAV and CoV infectionss.

Molecules/processes	Virus strain	Major findings	Ref.
Cell cycling proteins	IAV	Competitive inhibition of IAV M1–M2 interaction by cyclin D3 impairs infectious virus packaging, resulting in attenuation	[57]
Apoptosis-related signals	IAV	Apoptosis signaling modulates IAV propagation, innate host defense, and lung injury.	[60]
Sex hormones-related signals	IAV	Progesterone-based contraceptives reduce adaptive immune responses and protection against subsequent IAV infections.	[59]
	SARS-CoV	Male mice were more susceptible to SARS-CoV infection compared with age-matched females, while estrogen receptor signaling played a critical role in protecting females from SARS-CoV-mediated pathogenesis.	[53]
CHD chromatin remodeler	IAV	CHD1 is a proviral regulator of IAV multiplication.	[63]
Nuclear import and export machinery	IAV	IAV have evolved different mechanisms to utilize importin-alpha isoforms, affecting importation on both sides of the nuclear envelope.	[65]
		Activation of the interferon induction cascade by IAV requires viral RNA synthesis and nuclear export.	[61]
		Human heat shock protein 40 promotes IAV replication by assisting in the nuclear import of viral ribonucleoproteins.	[52]
		Preferential usage of importin-alpha7 isoforms by seasonal IAV in the human upper respiratory tract makes it a target of selective pressure.	[64]
Vesicular trafficking	IAV	IAV infection modulates vesicular trafficking and induces Golgi complex disruption.	[68]
		IAV enhances its propagation through modulating Annexin-A1 dependent endosomal trafficking.	[51]
		IAV ribonucleoproteins modulate host recycling by competing with Rab11 effectors.	[67]
	SARS-CoV	A predicted beta-hairpin structural motif in the cytoplasmic tail of the SARS-CoV E protein is sufficient for Golgi complex localization of a reporter protein and functions as a Golgi complex-targeting signal.	[54]
	MERS-CoV	CD9-facilitated condensation of receptors and proteases allows MERS-CoV pseudoviruses to enter cells rapidly and efficiently.	[56]
Exosome secretion	IAV	Exosome deficiency uncoupled chromatin targeting of the viral polymerase complex and the formation of cellular-viral RNA hybrids, which are essential RNA intermediates that license transcription of antisense genomic viral RNAs	[66]
Autophagy	IAV	Autophagy induction regulates IAV replication in a time-dependent manner.	[58]
	SARS-CoV	CoV nsp6 restricts autophagosome expansion.	[55]
Cellular senescence	IAV	Cellular senescence enhances viral replication.	[62]
Coagulation	IAV	Beneficial effects of inflammation-coagulation interactions during IAV infection	[69]