Viral strategies for triggering and manipulating mitophagy

Abstract

Viral infection causes many physiological alterations in the host cell, and many of these alterations can affect the host mitochondrial network, including mitophagy induction. A substantial amount of literature has been generated that advances our understanding of the relationship between mitophagy and several viruses. Some viruses trigger mitophagy directly, and indirectly and control the mitophagic process via different strategies. This enables viruses to promote persistent infection and attenuate the innate immune responses. In this review, we discuss the events of virus-regulated mitophagy and the functional relevance of mitophagy in the pathogenesis of viral infection and disease. Abbreviation: ATG: autophagy related; BCL2L13: BCL2 like 13; BNIP3L/NIX: BCL2 interacting protein 3 like; CL: cardiolipin; CSFV: classical swine fever virus; CVB: coxsackievirus B; DENV: dengue virus; DNM1L: dynamin 1 like; FIS1: fission, mitochondrial 1; FUNDC1: FUN14 domain containing 1; HPIV3: human parainfluenza virus 3; HSV-1: herpes simplex virus type 1; IMM: inner mitochondrial membrane; IAV: influenza A virus; IFN: interferon; IKBKE/IKKε: inhibitor of nuclear factor kappa B kinase subunit epsilon; LUBAC: linear ubiquitin assembly complex; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MeV: measles virus; MAVS: mitochondrial antiviral signaling protein; MFF: mitochondria fission factor; NLRP3: NLR family pyrin domain containing 3; NDV: Newcastle disease virus; NR4A1: nuclear receptor subfamily 4 group A member 1; OMM: outer mitochondrial membrane; OPA1: OPA1, mitochondrial dynamin like GTPase; PRKN: parkin RBR E3 ubiquitin protein ligase; PINK1: PTEN induced putative kinase 1; PHB2: prohibitin 2; PRRSV: porcine reproductive and respiratory syndrome virus; PRRs: pattern-recognition receptors; RLRs: RIG-I-like receptors; ROS: reactive oxygen species; RIPK2: receptor interacting serine/threonine kinase 2; SESN2: sestrin 2; SNAP29: synaptosome associated protein 29; STX17: syntaxin 17; TGEV: transmissible gastroenteritis virus; TUFM: Tu translation elongation factor, mitochondrial; TRAF2: TNF receptor associated factor 2; TRIM6: tripartite motif containing 6; Ub: ubiquitin; ULK1: unc-51 like autophagy activating kinase 1; VZV: varicella-zoster virus.

Immunological observations and transcriptomic analysis of trimester‐specific full‐term placentas from three Zika virus‐infected women

“…34 It is known that some viruses attack the host cell mitochondrial network as a form of immune evasion. 35,36 The findings described herein can be translated into the clinical prenatal screening procedures in ZIKV-infected or any arbovirus-infected pregnant patients. In such circumstances, abnormalities in the numbers of leucocytes 37,38 and biomarkers indicative of ongoing inflammation 39 or oxidative stress 40 and presence of any microbial infections 41 should be screened as advised by the clinic.…”

“…Mitochondrial dysfunction could also indicate an impairment of the antiviral immune response . It is known that some viruses attack the host cell mitochondrial network as a form of immune evasion …”

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

“…The relationship between mitophagy and innate immunity is discussed in recent review articles [84,97,[144][145][146][147]. The interaction between mitophagy and innate immunity is crucial for the host's protective response to infection.…”

The Glycoprotein and Nucleocapsid Protein of Hantaviruses Manipulate Autophagy Flux to Restrain Host Innate Immune Responses

“…Interacting with TUFM Mitochondrial sequestration by autophagosomes is a key step of mitophagy, which can be broadly classified into two distinct groups: Parkin dependent and Parkin independent. The former involves the selective tagging of impaired mitochondria by PTEN-induced putative kinase 1 (PINK1), which recruits the E3-ubiquitin ligase Parkin and results in subsequent mitochondrial sequestration within autophagosomes (Zhang et al, 2018). HeLa cells do not express endogenous Parkin (Lazarou et al, 2015), while Gn overexpression in HeLa cells still strongly induces the decrease in p62, Hsp60, TOM20, and TIM23 (Figure S3B), suggesting that Gn can induce complete mitophagy in the absence of Parkin.…”