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Keynote Presentation at the Eight International Congress of Behavioral Medicine: the Pittsburgh common cold studies: psychosocial predictors of susceptibility to respiratory infectious illness.

This article provides a selected overview of 20 years of research on the role of psychosocial factors in susceptibility to upper respiratory infections. We present evidence from our laboratory that psychological stress is associated with increased risk for developing respiratory illness for persons intentionally exposed to a common cold virus, that the longer the duration of the stressor the greater the risk, and that stress association with susceptibility may be mediated by stress-induced disruption of the regulation of proinflammatory cytokines. We further provide evidence that social relationships (social integration and social support) are also associated with risk for respiratory illness: Social integration is associated with reduced risk irrespective of stress level and social support protects persons from the pathogenic influences of stress. Finally, we report recent evidence that lower levels of early childhood socioeconomic status (SES) are associated with greater risk of viral-induced illness during adulthood, independent of adult SES.

Cytokines↗

[Assay for paracetamol by derivative spectrophotometry in compound amantadine tablets].

Compound amantadine tablets is a new drug for virus-common cold. It was consisted of paracetamol, amantadine hydrochloride and caffeine etc. Because of the disturbing of the caffeine, the paracetamol can not be determined by UV directly. So the paracetamol in compound amantadine tablets was determined by derivative spectrophotometry. This method is simple and rapid, no distillation and no separation, with average recovery of 100.0%, and RSD of 0.36%.

Acetaminophen↗

Stress and infections.

Neurotransmitters and neuroendocrine hormones can modify the functioning of immune cells and conversely cytokines produced by immune cells can alter brain homeostasis. This connection is further manifested by experimental studies showing a relationship between stress and resistance to infection. Human subjects with a high stress index were shown to be more susceptible to infection with common cold viruses. Furthermore, a diversity of experimental animal paradigms show that laboratory stressors such as forced exercise, avoidance learning, restraint, isolation, and cold exposure make animals more susceptible to primary infection with a variety of viruses and bacteria. The cellular and molecular basis for the observed modulation of host resistance is not fully understood but involves altered functioning of both T lymphocytes and cells of the hypothalamic-pituitary adrenal axis. Also involved is the altered production of cytokines and hormones produced by the immune system and brain.

Animals↗

Common community respiratory viruses in patients with cancer: more than just "common colds".

Community respiratory viruses long have been recognized as primary respiratory pathogens among infants and young children. More recently, it has become clear that these viruses cause a considerable disease burden throughout life. The consequences of repeated infections are most evident in elderly and immunocompromised persons. Even in otherwise healthy persons, reinfections often require medical attention but generally are undiagnosed and unrecognized. These reinfections may spread from healthy persons to those at highest risk. Control requires a multifaceted approach combining vaccination, chemoprophylaxis, and aggressive early antiviral treatment of high-risk individuals, as well as education of all populations affected by these viruses.

Community-Acquired Infections↗

Disrupted spatial memory is a consequence of picornavirus infection.

Picornaviruses are a socioeconomically important family of viruses that includes the rhinoviruses and enteroviruses. Many of these viruses, including the "common cold" Coxsackie virus A21, maintain neurovirulent potential and may induce hippocampal injury. The behavioral implications of this injury have not been adequately explored. Using C57BL/6J mice infected with Theiler's murine encephalomyelitis virus, we examined the formation of spatial memories using the Morris water maze test. Virus-infected mice had greater search error compared to sham-infected animals during the location of a hidden platform and were unable to discriminate the location of the training quadrant during the final probe trial. Furthermore, sham-infected mice were place responders whereas virus-infected mice were cue responders, indicating a lack of spatial memory formation in infected animals. Importantly, the degree of memory impairment was correlated to the extent of hippocampal injury. This suggests that picornavirus infection of the human CNS may also result in at least some degree of neurologic deficit. An important implication of such subclinical virus-induced neurologic deficit is that the injury may accumulate over the lifetime of the individual, eventually leading to the manifestation of clinical cognitive or memory deficits.

Animals↗

[Origin of SARS from accelerated evolution of a virus by combined pollution].

The SARS virus origin which obviously differs from the theory of out-space origin and the theory of wildlife origin was theoretically discussed based on principles of pollution-evolution ecology, pathogenesis and infectant characteristics of SARS, and some relevant experimental evidence. It emphasizes on the fact that increasingly combined pollution in China provides a substantial basis for virus evolution. Gene recombination and fusion of more than one virus in ecosystems should take charge with the origin of a SARS virus. In particular, a common cold or influenza virus can acceleratedly changed into a superpower common cold or influenza virus through genetic mutation and gene recombination by increasingly combined pollution. This work can be useful for human beings to overcome SARS in theory.

Animals↗