scholarly journals Role of CD25+ CD4+ T cells in acute and persistent coronavirus infection of the central nervous system

Virology ◽  
2013 ◽  
Vol 447 (1-2) ◽  
pp. 112-120 ◽  
Author(s):  
Maria Teresa P. de Aquino ◽  
Shweta S. Puntambekar ◽  
Carine Savarin ◽  
Cornelia C. Bergmann ◽  
Timothy W. Phares ◽  
...  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Cd4 T Cells ◽  
The Central Nervous System ◽  
Coronavirus Infection

scholarly journals The incidence and pathophysiology of neurological symptoms in COVID-19

2021 ◽  
Vol 40 (4) ◽  
pp. 33-42
Author(s):  
Igor V. Litvinenko ◽  
Miroslav M. Odinak ◽  
Nikolay V. Tsygan ◽  
Aleksander V. Ryabtsev
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Rare Complication ◽  
Cranial Nerves ◽  
Neurological Symptoms ◽  
Immune Mediated ◽  
High Incidence ◽  
The Central Nervous System ◽  
Coronavirus Infection

The central nervous system seems to be quite vulnerable to SARS-CoV-2, leading to a variety of alteration pathways, high incidence and variability of the neurological symptoms of COVID-19. The COVID-19 symptoms, possibly associated with alteration to the central nervous system, include hyperthermia, shortness of breath, fatigue, headache, dizziness, dysphonia, dysphagia, hyposmia and anosmia, hypogeusia and ageusia, impairment of consciousness. The impairment of olfaction and gustation are the most common symptoms of the nervous system alteration (98% and 70%, respectively), which is most likely a consequence of the alteration of the receptors. Presumably the pathogenesis of dysphonia and dysphagia may involve neurodegenerative mechanisms or may be associated with a predominantly demyelinating alteration of the caudal cranial nerves. Pathomorphological findings in the brain of the COVID-19 patients include diffuse hypoxic and focal ischemic injuries of various sizes up to ischemic infarctions (in thrombosis of large arteries); microangiopathy; vasculitis; diapedetic and confluent hemorrhages with possible progression to hemorrhagic infarctions and rarely intracerebral hematomas. Acute cerebrovascular accident worsens the course of COVID-19 and can worsen the clinical outcome, taking into account the mechanisms of the central nervous system alteration in highly contagious coronavirus infections (SARS-CoV, MERS, SARS-CoV-2), including embolism, hypoxia, neurodegeneration, systemic inflammatory response and immune-mediated alteartion to the nervous tissue. A fairly rare complication of coronavirus infection, however, acute myelitis requires attention due to the severity of neurological disorders. The literature data show high incidence and polymorphism of the symptoms of the central nervous system alteration, as well as the important role of the cerebrovascular and neurodegenerative pathogenesis of brain alteration in COVID-19, which is taken into account in examining and treating the patients with new coronavirus infection. (1 figure, bibliography: 61 refs)

scholarly journals Expanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System

2017 ◽  
Vol 8 ◽  
Author(s):  
Deepti Pilli ◽  
Alicia Zou ◽  
Fiona Tea ◽  
Russell C. Dale ◽  
Fabienne Brilot
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Autoimmune Diseases ◽  
The Central Nervous System

scholarly journals High-Magnitude, Virus-Specific CD4 T-Cell Response in the Central Nervous System of Coronavirus-Infected Mice

2001 ◽  
Vol 75 (6) ◽  
pp. 3043-3047 ◽  
Author(s):  
Jodie S. Haring ◽  
Lecia L. Pewe ◽  
Stanley Perlman
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Cd4 T Cells ◽  
Hepatitis Virus ◽  
T Cell Response ◽  
Acute Encephalitis ◽  
High Magnitude ◽  
The Central Nervous System ◽  
Ifn Γ

ABSTRACT The neurotropic JHM strain of mouse hepatitis virus (MHV) causes acute encephalitis and chronic demyelinating encephalomyelitis in rodents. Previous results indicated that CD8 T cells infiltrating the central nervous system (CNS) were largely antigen specific in both diseases. Herein we show that by 7 days postinoculation, nearly 30% of the CD4 T cells in the acutely infected CNS were MHV specific by using intracellular gamma interferon (IFN-γ) staining assays. In mice with chronic demyelination, 10 to 15% of the CD4 T cells secreted IFN-γ in response to MHV-specific peptides. Thus, these results show that infection of the CNS is characterized by a large influx of CD4 T cells specific for MHV and that these cells remain functional, as measured by cytokine secretion, in mice with chronic demyelination.

Maintenance of CD8+T Cells during Acute Viral Infection of the Central Nervous System Requires CD4+T Cells But Not Interleukin-2

2005 ◽  
Vol 18 (1) ◽  
pp. 162-169 ◽  
Author(s):  
Jiehao Zhou ◽  
David R. Hinton ◽  
Stephen A. Stohlman ◽  
Chih-Pin Liu ◽  
Lingwen Zhong ◽  
...  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Viral Infection ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Interleukin 2 ◽  
Acute Viral Infection ◽  
The Central Nervous System

scholarly journals CD4+ T-Cell Responses Are Required for Clearance of West Nile Virus from the Central Nervous System

2006 ◽  
Vol 80 (24) ◽  
pp. 12060-12069 ◽  
Author(s):  
Elizabeth M. Sitati ◽  
Michael S. Diamond
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
West Nile Virus ◽  
T Cell ◽  
Wild Type ◽  
Cell Responses ◽  
The Central Nervous System ◽  
Deficient Mice

ABSTRACT Although studies have established that innate and adaptive immune responses are important in controlling West Nile virus (WNV) infection, the function of CD4+ T lymphocytes in modulating viral pathogenesis is less well characterized. Using a mouse model, we examined the role of CD4+ T cells in coordinating protection against WNV infection. A genetic or acquired deficiency of CD4+ T cells resulted in a protracted WNV infection in the central nervous system (CNS) that culminated in uniform lethality by 50 days after infection. Mice surviving past day 10 had high-level persistent WNV infection in the CNS compared to wild-type mice, even 45 days following infection. The absence of CD4+ T-cell help did not affect the kinetics of WNV infection in the spleen and serum, suggesting a role for CD4-independent clearance mechanisms in peripheral tissues. WNV-specific immunoglobulin M (IgM) levels were similar to those of wild-type mice in CD4-deficient mice early during infection but dropped ∼20-fold at day 15 postinfection, whereas IgG levels in CD4-deficient mice were ∼100- to 1,000-fold lower than in wild-type mice throughout the course of infection. WNV-specific CD8+ T-cell activation and trafficking to the CNS were unaffected by the absence of CD4+ T cells at day 9 postinfection but were markedly compromised at day 15. Our experiments suggest that the dominant protective role of CD4+ T cells during primary WNV infection is to provide help for antibody responses and sustain WNV-specific CD8+ T-cell responses in the CNS that enable viral clearance.

scholarly journals Role of Viral Persistence in Retaining CD8+ T Cells within the Central Nervous System

2000 ◽  
Vol 74 (17) ◽  
pp. 7903-7910 ◽  
Author(s):  
Norman W. Marten ◽  
Stephen A. Stohlman ◽  
Cornelia C. Bergmann
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Hepatitis Virus ◽  
Viral Persistence ◽  
Viral Rna ◽  
Cns Infection ◽  
Organ Specific ◽  
The Central Nervous System

ABSTRACT The continued presence of virus-specific CD8+ T cells within the central nervous system (CNS) following resolution of acute viral encephalomyelitis implicates organ-specific retention. The role of viral persistence in locally maintaining T cells was investigated by infecting mice with either a demyelinating, paralytic (V-1) or nonpathogenic (V-2) variant of a neurotropic mouse hepatitis virus, which differ in the ability to persist within the CNS. Class I tetramer technology revealed more infiltrating virus-specific CD8+ T cells during acute V-1 compared to V-2 infection. However, both total and virus-specific CD8+ T cells accumulated at similar peak levels in spinal cords by day 10 postinfection (p.i.). Decreasing viral RNA levels in both brains and spinal cords following initial virus clearance coincided with an overall progressive loss of both total and virus-specific CD8+ T cells. By 9 weeks p.i., T cells had largely disappeared from brains of both infected groups, consistent with the decline of viral RNA. T cells also completely disappeared from V-2-infected spinal cords coincident with the absence of viral RNA. By contrast, a significant number of CD8+ T cells which contained detectable viral RNA were recovered from spinal cords of V-1-infected mice. The data indicate that residual virus from a primary CNS infection is a vital component in mediating local retention of both CD8+ and CD4+ T cells and that once minimal thresholds of stimuli are lost, T cells within the CNS cannot survive in an autonomous fashion.

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