[53, 54] Infection of the central nervous system (CNS) by hRSV ha

[53, 54] Infection of the central nervous system (CNS) by hRSV has been supported by the presence of viral RNA in human cerebrospinal fluid,[53] which correlates with neurological symptoms including seizures, central apnoea, lethargy, feeding or swallowing difficulties, abnormalities of muscle tone, strabismus, abnormalities

of the cerebrospinal fluid and encephalopathy.[54] Our group evaluated whether the CNS of mice and rats challenged with hRSV can be reached by this virus after intranasal infection.[55] The presence of hRSV was corroborated in brain tissues using immunofluorescence and real-time PCR assays, which showed hRSV proteins and nucleic acids in several zones of the brain, supporting PF-02341066 research buy the notion that hRSV infection reaches the CNS.[55] Entrance of

hRSV to Ivacaftor chemical structure the CNS was dependent on the blood–brain barrier, because the blockade of CD49d by a monoclonal antibody that targets integrin α4 and impairs leucocyte extravasation through the blood–brain barrier decreased viral loads in the brain but not in the lungs.[55] As a result of hRSV infection, impairment in cognition was revealed in rodents submitted to water-maze as a spatial learning test and to marble burying as a behavioural test.[55] These alterations were correlated with electrophysiological studies that showed an impairment in the induction of long-term potentiation in stratum radiatum at the hippocampus area.[55] Together, these observations support the previously described notion that hRSV has the ability to infect CNS tissues in a disseminated pattern and that this virus is capable of disrupting cognitive functions by altering

the synaptic plasticity of the infected brain tissue.[55] Human RAS p21 protein activator 1 RSV is considered an important health burden affecting mainly children and the elderly. Unfortunately, currently available treatments for infections by this pathogen are limited and it is not possible to use them broadly because of their high cost. However, there are many efforts invested in the design of new drugs to control the symptoms and unwanted effects caused by hRSV infection. The knowledge of the life cycle of hRSV and the pathology induced in the infected host is essential for the design of drugs with curative or prophylactic purposes. Along these lines, the most relevant processes in the life cycle of hRSV are replication, transcription and fusion, which are potential targets for antiviral drugs.[56] Table 1 summarizes the antiviral drugs designed up to date against hRSV infection.

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