Viral Infections and Brain Development

Neuroinflammation and Brain Development: Possible Risk Factors in COVID-19-Infected Children

NeuroImmunoModulation ◽

10.1159/000512815 ◽

2021 ◽

pp. 1-7

Author(s):

Luana da Silva Chagas ◽

Poliana Capucho Sandre ◽

Patricia Coelho de Velasco ◽

Henrique Marcondes ◽

Natalia Cristina Aparecida Ribeiro e Ribeiro ◽

...

Keyword(s):

Risk Factors ◽

Fatty Acids ◽

Brain Development ◽

Neural Development ◽

Viral Infections ◽

Additional Risk ◽

Autoimmune Hypothyroidism ◽

Inflammatory Syndrome ◽

Nutritional Imbalance ◽

Synaptic Pruning

COVID-19, a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) betacoronavirus, affects children in a different way than it does in adults, with milder symptoms. However, several cases of neurological symptoms with neuroinflammatory syndromes, such as the multisystem inflammatory syndrome (MIS-C), following mild cases, have been reported. As with other viral infections, such as rubella, influenza, and cytomegalovirus, SARS-CoV-2 induces a surge of proinflammatory cytokines that affect microglial function, which can be harmful to brain development. Along with the viral induction of neuroinflammation, other noninfectious conditions may interact to produce additional inflammation, such as the nutritional imbalance of fatty acids and polyunsaturated fatty acids and alcohol consumption during pregnancy. Additionally, transient thyrotoxicosis induced by SARS-CoV-2 with secondary autoimmune hypothyroidism has been reported, which could go undetected during pregnancy. Together, those factors may pose additional risk factors for SARS-CoV-2 infection impacting mechanisms of neural development such as synaptic pruning and neural circuitry formation. The present review discusses those conditions in the perspective of the understanding of risk factors that should be considered and the possible emergence of neurodevelopmental disorders in COVID-19-infected children.

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Viral Infections and Brain Development

Brain Fetal and Infant ◽

10.1007/978-94-009-9680-9_14 ◽

1977 ◽

pp. 213-223

Author(s):

Richard T. Johnson

Keyword(s):

Brain Development ◽

Viral Infections

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Lessons From Zika and Other Virus Induced Skull Deformity

FACE ◽

10.1177/2732501620939515 ◽

2020 ◽

Vol 1 (1) ◽

pp. 44-50

Author(s):

Mohamad Masoumy ◽

Emily P. Masoumy ◽

Babak Baban ◽

Jack C. Yu

Keyword(s):

Brain Development ◽

Immune Activation ◽

Viral Infections ◽

Fetal Brain ◽

Growth Dynamics ◽

Cell Loss ◽

Maternal Immune Activation ◽

Skull Deformity ◽

Critical Phases ◽

The Impact

Objective: Viral infections during pregnancy can cause disturbance in normal craniofacial morphogenesis. While some pathogens such as cytomegalovirus and herpes simplex are familiar to us, others remain obscure. This review examines the arbovirus-induced cranial deformities and combines biomechanics with growth dynamics to gain a deeper appreciation of this complex morphogenetic process. Materials and Methods: Using Wolfram Alpha, we analyzed the impact of cell population changes. The growth dynamics of the brain, and thus the size of the calvarium, followed 2 potential logistic curves: compensated and uncompensated. To understand the potential mechanism of cell loss, we performed literature review on maternal immune activation and viral tropism for neurons and glial cells. Results: With arboviral infections such as Zika, uncompensated loss of cells during the critical phases of fetal brain development reduces the intracranial mass and therefore decreases the tensile stress across the cranial sutures. The deflationary effect produces microcephaly by subduction and reduced osteogenesis seen clinically in these infants. Conclusion: Many viral infections cause intense maternal immune activation, some have neurotropism and can result in cell loss within the developing cranium. Unable to overcome this loss, the cranium assumes a new, abnormal shape and volume. Secondary calvarial deformities is due to, and should not cause, changes in brain development.

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The Diagnosis of Viral Disease by Electron Microscopy

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010005398x ◽

1982 ◽

Vol 40 ◽

pp. 270-273

Author(s):

William B. McCombs ◽

Cameron E. McCoy

Keyword(s):

Electron Microscopy ◽

Hospital Stay ◽

Viral Infections ◽

Medical Profession ◽

Bacterial Pathogens ◽

Viral Disease ◽

Viral Pathogens ◽

Academic Interest ◽

The Past

Recent years have brought a reversal in the attitude of the medical profession toward the diagnosis of viral infections. Identification of bacterial pathogens was formerly thought to be faster than identification of viral pathogens. Viral identification was dismissed as being of academic interest or for confirming the presence of an epidemic, because the patient would recover or die before this could be accomplished. In the past 10 years, the goal of virologists has been to present the clinician with a viral identification in a matter of hours. This fast diagnosis has the potential for shortening the patient's hospital stay and preventing the administering of toxic and/or expensive antibiotics of no benefit to the patient.

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Detection of Nucleic Acids in Cells or Tissue Sections Using In situ Polymerase Chain Reaction (PCR)

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100162545 ◽

1996 ◽

Vol 54 ◽

pp. 16-17

Author(s):

J. R. Hully ◽

K. R. Luehrsen ◽

K. Aoyagi ◽

C. Shoemaker ◽

R. Abramson

Keyword(s):

Nucleic Acids ◽

Viral Infections ◽

Anatomical Location ◽

Rt Pcr ◽

Reverse Transcription Pcr ◽

Cellular Source ◽

Gene Transcripts ◽

Initial Description ◽

In Cells

The development of PCR technology has greatly accelerated medical research at the genetic and molecular levels. Until recently, the inherent sensitivity of this technique has been limited to isolated preparations of nucleic acids which lack or at best have limited morphological information. With the obvious exception of cell lines, traditional PCR or reverse transcription-PCR (RT-PCR) cannot identify the cellular source of the amplified product. In contrast, in situ hybridization (ISH) by definition, defines the anatomical location of a gene and/or it’s product. However, this technique lacks the sensitivity of PCR and cannot routinely detect less than 10 to 20 copies per cell. Consequently, the localization of rare transcripts, latent viral infections, foreign or altered genes cannot be identified by this technique. In situ PCR or in situ RT-PCR is a combination of the two techniques, exploiting the sensitivity of PCR and the anatomical definition provided by ISH. Since it’s initial description considerable advances have been made in the application of in situ PCR, improvements in protocols, and the development of hardware dedicated to in situ PCR using conventional microscope slides. Our understanding of the importance of viral latency or viral burden in regards to HIV, HPV, and KSHV infections has benefited from this technique, enabling detection of single viral copies in cells or tissue otherwise thought to be normal. Clearly, this technique will be useful tool in pathobiology especially carcinogenesis, gene therapy and manipulations, the study of rare gene transcripts, and forensics.

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