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Publisher Summary This chapter discusses the general mechanisms of antiviral resistance. Mammalian viruses represent a diverse group of infectious agents. The viruses that cause the common diseases of man and domestic animals comprise approximately 25 known families, which fall into groups according to their genome and replication strategies. Further evolution of modern viruses is continuing with mutations, recombinations, or reassortments. The use of vaccines has greatly reduced the burden of human disease caused by several other human viruses. Specific antiviral compounds have been developed for several of those viral infections that have not been adequately controlled by vaccines. Herpes viruses establish a latent state that enables the virus to remain in the host for a lifetime despite normal adaptive immune responses. Antivirals are effective at reducing virus replication during an acute episode. Another way in which a virus can establish a form of latency is by means of integration of a DNA copy of the genome. The virus has over 100 serotypes/genotypes. The mutation rate of a virus has been described as the probability that during a single replication of the virus genome a particular nucleotide position is altered. Several families of RNA virus have segmented genomes. Resistant variants are selected so quickly that a treated person can pass on resistant virus to contacts. Viruses are resistant to specific antiviral drugs. Although the genetic barrier needs to be increased for long-term delay in resistance in chronic infections, with any drug combination used in naturally self-limiting infections, the extra effect in reducing viral load quickly may well be a useful benefit. Our current antiviral therapies have been successful in reducing the burden of human diseases but many viruses have evolved strategies for countering new threats to their replication. |
