Not sure if posted but this is a good one for CCL5 and it's receptors.
https://www.tandfonline.com/doi/full/10.1517/...ecsys&
In conclusion, in the context of respiratory and neurotropic viral infections, it seems that CCL5 production presents a dual role. CCL5 is necessary to control certain viral infection, including influenza, RSV, RV, HSV and WNV. The antiviral role of CCL5 is evident in HHV-8 and HCMV infections, where immune evasion mechanisms targeting CCL5 are essential and actively employed by these viruses. However, CCL5 seems to be deleterious in later phases of infection, where it contributes to excessive inflammation and tissue damage in all the diseases addressed in this section. Thus, conceptually, it would be ideal to block CCL5 in later phases of infection, where immunopathology is the main component of respiratory or neurotropic diseases, rather than the virus itself. The role of CCL5 in liver infections is not as clear, especially because beneficial or detrimental effects of CCL5 are dependent on the chemokine receptor engaged and whether the infection is chronic (viral hepatitis) or acute (YFV and DENV). However, CCL5-mediated inflammation is a common feature of these infections in later phases, which contributes to fibrosis or to hemorrhagic manifestations depending on the infection. Therefore, any potential blockade of CCL5 or its receptors in the context of viral infections could only be employed at the later stages of disease in order to prevent immunopathology. Earlier treatment could have deleterious effects on the capacity of the host to deal with the viral infection. As separating early (viral-mediated) and late (immune-mediated) phases of disease after viral infection may be very problematic in the clinical context, it is not likely that strategies aimed at blocking CCL5 or its receptors may be useful in patients. The clear exception is HIV as in this case blockade of CCR5 is associated with decreased viral entry. Blocking CCL5 in the context of HIV is unlikely to achieve similar benefits.
https://www.tandfonline.com/doi/full/10.1517/...ecsys&
In conclusion, in the context of respiratory and neurotropic viral infections, it seems that CCL5 production presents a dual role. CCL5 is necessary to control certain viral infection, including influenza, RSV, RV, HSV and WNV. The antiviral role of CCL5 is evident in HHV-8 and HCMV infections, where immune evasion mechanisms targeting CCL5 are essential and actively employed by these viruses. However, CCL5 seems to be deleterious in later phases of infection, where it contributes to excessive inflammation and tissue damage in all the diseases addressed in this section. Thus, conceptually, it would be ideal to block CCL5 in later phases of infection, where immunopathology is the main component of respiratory or neurotropic diseases, rather than the virus itself. The role of CCL5 in liver infections is not as clear, especially because beneficial or detrimental effects of CCL5 are dependent on the chemokine receptor engaged and whether the infection is chronic (viral hepatitis) or acute (YFV and DENV). However, CCL5-mediated inflammation is a common feature of these infections in later phases, which contributes to fibrosis or to hemorrhagic manifestations depending on the infection. Therefore, any potential blockade of CCL5 or its receptors in the context of viral infections could only be employed at the later stages of disease in order to prevent immunopathology. Earlier treatment could have deleterious effects on the capacity of the host to deal with the viral infection. As separating early (viral-mediated) and late (immune-mediated) phases of disease after viral infection may be very problematic in the clinical context, it is not likely that strategies aimed at blocking CCL5 or its receptors may be useful in patients. The clear exception is HIV as in this case blockade of CCR5 is associated with decreased viral entry. Blocking CCL5 in the context of HIV is unlikely to achieve similar benefits.
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