Influenza virus A(H3N2) strain isolated from cerebrospinal fluid from a patient presenting myelopathy post infectious

Paiva, T. M. N.; Theotonio, G.; Paulino, R.S.; Benega, Margareth Aparecida; Silva, D.B.B.; Borborema, Samanta Etel Treiger; Ikeda, Takeshi; Kisielius, Jonas José; Ueda, Mirthes; Oliveira, Maria Isabel de; Santos, C.

doi:10.1016/j.jcv.2013.05.021

Cited by 3 publications

(4 citation statements)

References 7 publications

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“…Moreover, although in this study the detection methodology for IV genetic material detection in CSF was improved, only one sample was positive (Steininger et al, 2003 ; Figure 2 ). In another approximation to understand the etiologic agent causing myelopathy post-influenza-like syndrome, CSF obtained from a patient with this disease was inoculated in several cell lines, previously reported to be permissive for the growth of this virus (Paiva et al, 2013 ). Importantly, seasonal IAV H3N2 was detected in MDCK cells, identified as the cause of the neurological symptoms of the patient (Paiva et al, 2013 ).…”

Section: Influenza Virusmentioning

confidence: 99%

“…In another approximation to understand the etiologic agent causing myelopathy post-influenza-like syndrome, CSF obtained from a patient with this disease was inoculated in several cell lines, previously reported to be permissive for the growth of this virus (Paiva et al, 2013 ). Importantly, seasonal IAV H3N2 was detected in MDCK cells, identified as the cause of the neurological symptoms of the patient (Paiva et al, 2013 ). Besides the main symptoms reported for seasonal H1N1, H3N2 and IBV, altered state of consciousness are consistently detected with seizures, in patients infected with pandemics IAV subtypes (Newland et al, 2003 ; Popescu et al, 2017 ; Paksu et al, 2018 ).…”

Section: Influenza Virusmentioning

confidence: 99%

“…Both in this and in others studies, it has been difficult to correlate clinical signs such as CSF pleocytosis with neurological manifestation; mainly due to the low number of patients that exhibit pleocytosis (Paksu et al, 2018 ). However, the presence of neuroradiological diagnosis suggests that the phenotype observed in patients may be a cause of direct viral invasion into the CNS (Paiva et al, 2013 ; Paksu et al, 2018 ). Besides the neurological signs described above, a study in Japan reveals that patients with neurological manifestations also had mild impairment of consciousness, typically delirium or hallucinations and abnormal behavior among others, which belongs to the neuropsychiatric disorders (Manjunatha et al, 2011 ; Mizuguchi, 2013 ).…”

Section: Influenza Virusmentioning

confidence: 99%

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Neurologic Alterations Due to Respiratory Virus Infections

Böhmwald

Gálvez

Ríos

et al. 2018

Front. Cell. Neurosci.

561

587

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Central Nervous System (CNS) infections are one of the most critical problems in public health, as frequently patients exhibit neurologic sequelae. Usually, CNS pathologies are caused by known neurotropic viruses such as measles virus (MV), herpes virus and human immunodeficiency virus (HIV), among others. However, nowadays respiratory viruses have placed themselves as relevant agents responsible for CNS pathologies. Among these neuropathological viruses are the human respiratory syncytial virus (hRSV), the influenza virus (IV), the coronavirus (CoV) and the human metapneumovirus (hMPV). These viral agents are leading causes of acute respiratory infections every year affecting mainly children under 5 years old and also the elderly. Up to date, several reports have described the association between respiratory viral infections with neurological symptoms. The most frequent clinical manifestations described in these patients are febrile or afebrile seizures, status epilepticus, encephalopathies and encephalitis. All these viruses have been found in cerebrospinal fluid (CSF), which suggests that all these pathogens, once in the lungs, can spread throughout the body and eventually reach the CNS. The current knowledge about the mechanisms and routes used by these neuro-invasive viruses remains scarce. In this review article, we describe the most recent findings associated to neurologic complications, along with data about the possible invasion routes of these viruses in humans and their various effects on the CNS, as studied in animal models.

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Section: Influenza Virusmentioning

confidence: 99%

Section: Influenza Virusmentioning

confidence: 99%

Section: Influenza Virusmentioning

confidence: 99%

See 1 more Smart Citation

Neurologic Alterations Due to Respiratory Virus Infections

Böhmwald

Gálvez

Ríos

et al. 2018

Front. Cell. Neurosci.

561

587

View full text Add to dashboard Cite

show abstract

“…Previous studies have reported that during influenza virus infection there is an increase in the levels of proinflammatory cytokines, such as IL-1b, IL-6, CXCL8, CXCL9, CXCL10, CCL2, and TNF-a, in the CSF of patients who present neurological alterations such as acute encephalitis and encephalopathy (134,135). It is also known that patients infected with human orthopneumovirus and presenting neurological symptoms such as encephalitis and encephalopathies, have elevated levels of the proinflammatory cytokines IL-6, IL-8, CCL2, and CCL4 in CSF samples (136,137).…”

Section: Neurological Affectation Upregulated Cytokines Referencesmentioning

confidence: 99%

The relationship between chronic immune response and neurodegenerative damage in long COVID-19

et al. 2022

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In the past two years, the world has faced the pandemic caused by the severe acute respiratory syndrome 2 coronavirus (SARS-CoV-2), which by August of 2022 has infected around 619 million people and caused the death of 6.55 million individuals globally. Although SARS-CoV-2 mainly affects the respiratory tract level, there are several reports, indicating that other organs such as the heart, kidney, pancreas, and brain can also be damaged. A characteristic observed in blood serum samples of patients suffering COVID-19 disease in moderate and severe stages, is a significant increase in proinflammatory cytokines such as interferon-α (IFN-α), interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6) and interleukin-18 (IL-18), as well as the presence of autoantibodies against interferon-α (IFN-α), interferon-λ (IFN-λ), C-C motif chemokine ligand 26 (CCL26), CXC motif chemokine ligand 12 (CXCL12), family with sequence similarity 19 (chemokine (C-C motif)-like) member A4 (FAM19A4), and C-C motif chemokine ligand 1 (CCL1). Interestingly, it has been described that the chronic cytokinemia is related to alterations of blood-brain barrier (BBB) permeability and induction of neurotoxicity. Furthermore, the generation of autoantibodies affects processes such as neurogenesis, neuronal repair, chemotaxis and the optimal microglia function. These observations support the notion that COVID-19 patients who survived the disease present neurological sequelae and neuropsychiatric disorders. The goal of this review is to explore the relationship between inflammatory and humoral immune markers and the major neurological damage manifested in post-COVID-19 patients.

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Contribution of Pro-Inflammatory Molecules Induced by Respiratory Virus Infections to Neurological Disorders

2021

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Neurobehavioral alterations and cognitive impairment are common phenomena that represent neuropsychiatric disorders and can be triggered by an exacerbated immune response against pathogens, brain injury, or autoimmune diseases. Pro-inflammatory molecules, such as cytokines and chemokines, are produced in the brain by resident cells, mainly by microglia and astrocytes. Brain infiltrating immune cells constitutes another source of these molecules, contributing to an impaired neurological synapse function, affecting typical neurobehavioral and cognitive performance. Currently, there is increasing evidence supporting the notion that behavioral alterations and cognitive impairment can be associated with respiratory viral infections, such as human respiratory syncytial virus, influenza, and SARS-COV-2, which are responsible for endemic, epidemic, or pandemic outbreak mainly in the winter season. This article will review the brain′s pro-inflammatory response due to infection by three highly contagious respiratory viruses that are the leading cause of acute respiratory illness, morbidity, and mobility in infants, immunocompromised and elderly population. How these respiratory viral pathogens induce increased secretion of pro-inflammatory molecules and their relationship with the alterations at a behavioral and cognitive level will be discussed.

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Influenza virus A(H3N2) strain isolated from cerebrospinal fluid from a patient presenting myelopathy post infectious

Abstract: This study demonstrates that influenza virus A(H3N2) strain was the cause of illness of the students. According to the Brazilian influenza virus sentinel surveillance data A/Perth/16/2009-LIKE (H3N2) strain has predominated during the 2010 influenza virus season in Brasília-DF.

Cited by 3 publications

References 7 publications

Neurologic Alterations Due to Respiratory Virus Infections

Neurologic Alterations Due to Respiratory Virus Infections

The relationship between chronic immune response and neurodegenerative damage in long COVID-19

Contribution of Pro-Inflammatory Molecules Induced by Respiratory Virus Infections to Neurological Disorders

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