Apoptosis and microglial activation in influenza encephalopathy

Nakai, Yoshiko; Itoh, Masayuki; Mizuguchi, Masashi; Ozawa, Hiroshi; Okazaki, Etsuo; Kobayashi, Yasutsugu; Takahashi, Mitsuo; Ohtani, Kyoichi; Narita, Masahiko; Togashi, Takehiro; Takashima, Sachio

doi:10.1007/s00401-002-0605-x

Cited by 78 publications

(47 citation statements)

References 23 publications

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“…Apoptosis induced by coronaviral infection could be associated with HCoV-mediated neuropathogenesis by killing cells or by disseminating virus while limiting inflammatory responses. Indeed, neuronal apoptosis seems to represent an important contributing factor to acute CNS injury in humans after viral infection (DeBiasi et al, 2002;Nakai et al, 2003) and in HIV-associated dementia (Garden, 2002;Kolson, 2002).…”

Section: Discussionmentioning

confidence: 99%

Human coronavirus OC43 infection induces chronic encephalitis leading to disabilities in BALB/C mice

et al. 2006

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The notion that an infectious respiratory pathogen can damage the central nervous system (CNS) and lead to neurological disease was tested using a human respiratory coronavirus, the OC43 strain of human coronavirus (HCoV-OC43). First, primary cell cultures were used to determine the susceptibility of each type of neural cells to virus infection. Neurons were the target cells, undergoing degeneration during infection, in part due to apoptosis. Second, neuropathogenicity was investigated in susceptible mice. Intracerebral inoculation of HCoV-OC43 into BALB/c mice led to an acute encephalitis with neuronal cell death by necrosis and apoptosis. Infectious virus was apparently cleared from surviving animals, whereas viral RNA persisted for several months. Some of the animals surviving to acute encephalitis presented an abnormal limb clasping reflex and a decrease in motor activity starting several months post-infection. These results suggest that viral persistence could be associated with an increased neuronal degeneration leading to neuropathology and motor deficits in susceptible individuals.

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Section: Discussionmentioning

confidence: 99%

Human coronavirus OC43 infection induces chronic encephalitis leading to disabilities in BALB/C mice

et al. 2006

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“…Apoptosis has also been identified in the brains of influenza encephalopathy and encephalitis patients [304]. Microglial cells were markedly increased in TUNEL-positive influenza encephalopathy and encephalitis brains compared with TUNEL-negative brains.…”

Section: Infectious Agents and Neurodegenerative Processesmentioning

confidence: 99%

Infectious Agents and Neurodegeneration

Chiara

Marcocci

Sgarbanti³

et al. 2012

Mol Neurobiol

201

172

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A growing body of epidemiologic and experimental data point to chronic bacterial and viral infections as possible risk factors for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Infections of the central nervous system, especially those characterized by a chronic progressive course, may produce multiple damage in infected and neighbouring cells. The activation of inflammatory processes and host immune responses cause chronic damage resulting in alterations of neuronal function and viability, but different pathogens can also directly trigger neurotoxic pathways. Indeed, viral and microbial agents have been reported to produce molecular hallmarks of neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in synergy with other recognized risk factors, such as aging, concomitant metabolic diseases and the host’s specific genetic signature. This review will focus on the contribution given to neurodegeneration by herpes simplex type-1, human immunodeficiency and influenza viruses, and by Chlamydia pneumoniae.

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“…These foci have necrotic cells, localized edema, congestion and hemorrhages, but have little inflammation in the lesions or meninges (Yagishita et al, 1995;Sazgar et al, 2003;Togashi et al, 2004;Kirton et al, 2005;Lyon et al, 2010). One study reported histologic markers of apoptosis occurring in neurons and glia (Takahashi et al, 2000;Nakai et al, 2003). The cerebral blood vessels are not occluded by inflammatory cells or other debris but often had dilated Virchow-Robin spaces containing clear fluid (Ishigami et al, 2004).…”

Section: Acute Necrotizing Encephalopathyassociated With Influenzamentioning

confidence: 99%