Abstract
Virus infections are a major global public health concern, and only via substantial knowledge of virus pathogenesis and antiviral immune responses can we develop and improve medical treatments, and preventive and therapeutic vaccines. Innate immunity and the shaping of efficient early immune responses are essential for control of viral infections. In order to trigger an efficient antiviral defense, the host senses the invading microbe via pattern recognition receptors (PRRs), recognizing distinct conserved pathogen-associated molecular patterns (PAMPs). The innate sensing of the invading virus results in intracellular signal transduction and subsequent production of interferons (IFNs) and proinflammatory cytokines. Cytokines, including IFNs and chemokines, are vital molecules of antiviral defense regulating cell activation, differentiation of cells, and, not least, exerting direct antiviral effects. Cytokines shape and modulate the immune response and IFNs are principle antiviral mediators initiating antiviral response through induction of antiviral proteins. In the present review, I describe and discuss the current knowledge on early virus–host interactions, focusing on early recognition of virus infection and the resulting expression of type I and type III IFNs, proinflammatory cytokines, and intracellular antiviral mediators. In addition, the review elucidates how targeted stimulation of innate sensors, such as toll-like receptors (TLRs) and intracellular RNA and DNA sensors, may be used therapeutically. Moreover, I present and discuss data showing how current antimicrobial therapies, including antibiotics and antiviral medication, may interfere with, or improve, immune response.
Highlights
Present and emerging viral infections pose an increasing burden to public health, and significant resources are used to limit the spread of virus infections
Future research will have to delineate whether some of the reported virus-induced immune responses mediated via TLR2 and TLR4 are due to recognition of danger-associated molecular patterns (DAMPs) rather than direct recognition of the viruses, and further characterize the role of TLR2 and TLR4 during virus infection in humans
No CTR-induced activation of nuclear factor B (NF- B) or IFN regulatory factor 3 (IRF3) and subsequent IFN production has been shown during virus infection; CLR may induce signaling via a number of kinases, including spleen tyrosin kinase (SYK) and Src kinase during bacterial and virus infections; CLRs possibly shape innate responses during infection [72]
Summary
Present and emerging viral infections pose an increasing burden to public health, and significant resources are used to limit the spread of virus infections. The lack of efficient vaccines for many viral infections, the suboptimal treatment for many viral infections, and the impact of viruses on human health and economy emphasize the need for an improved understanding of viruses’ natural history, including how the innate and adaptive immune responses may restrict virus infections, as well as modulate viral pathogenesis. The innate immune system is the very first line of defense, and early recognition of invading pathogens is essential to initiate an antiviral response. The inflammatory response induced by virus recognition may be detrimental to the host mediating immune-pathogenesis. The review addresses innate stimulation as a mean of improving vaccine responses or as a direct antiviral mediator. The review discusses how current antimicrobial therapies may regulate innate responses and possibly interfere with or improve pathogen clearance
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