sometimes transform host cells into cancer cells. viruses such as the human papillomavirus (hpv), human t-lymphotropic virus (htlv) etc., can stimulate growth of tumours in infected hosts, either by disrupting tumour suppressor gene expression (hpv) or upregulating proto-oncogene expression (htlv). damage caused by host immune system sometimes, instead of cell death or cellular dysfunction caused by the virus, the host immune response can mediate disease and excessive inflammation. the stimulation of the innate and adaptive immune system in response to viral infections destroys infected cells, which may lead to severe pathological consequences to the host. this damage caused by the immune system is known as virus-induced immunopathology. specifically, immunopathology is caused by the excessive release of antibodies, interferons and pro-inflammatory cytokines, activation of the complement system, or hyperactivity of cytotoxic t cells. secretion of interferons and other cytokines can trigger cell damage, fever and flu-like symptoms. in severe cases of certain viral infections, as in avian h5n1 influenza in 2005, aberrant induction of the host immune response can elicit a flaring release of cytokines known as a cytokine storm. in some instances, viral infection can initiate an autoimmune response, which occurs via different proposed mechanisms: molecular mimicry and bystander mechanism. molecular mimicry refers to an overlap in structural similarity between a viral antigen and a self-antigen. the bystander mechanism hypothesizes the initiation of a non-specific and overreactive antiviral response that tackles self-antigens in the process. damage caused by the host itself due to autoimmunity was observed in the west nile virus. incubation period viruses display variable incubation periods upon virus entry into the host. the incubation period refers to the time taken for the onset of disease after first contact with the virus. in rabiesvirus, the incubation period varies with the distance traversed by the virus to the target organ; but in most viruses the length of incubation depends on many factors. surprisingly, generalised infections by togaviruses have a short incubation period due to the direct entry of the virus into target cells through insect bites. there are several other factors that affect the incubation period. the mechanisms behind long incubation periods, months or years for example, are not completely understood yet. evolution of virulence some relatively avirulent viruses in their natural host show increased virulence upon transfer to a new host species. when an emerging virus first invades a new host species, the hosts have little or no immunity against the virus and often experience high mortality. over time, a decrease in virulence in the predominant strain can sometimes be observed. a successful pathogen needs to spread to at least one other host, and lower virulence can result in higher transmission rates under some circumstances. likewise, genetic resistance against the virus can develop in a host population over time. an example of the evolution of virulence in emerging virus is the case of myxomatosis in rabbits. the release of wild european rabbits in 1859 into victoria, australia for sport resulted in a rabbit plague. in order to curb with rabbit overpopulation, myxoma virus, a lethal species-specific poxvirus responsible for myxomatosis in rabbits, was deliberately released in south australia in 1950. this led to a 90% decrease in rabbit populations, and the disease became endemic in a span of five years. significantly, severely attenuated strains of the myxoma virus were detected in merely 2 years of its release, and genetic resistance in rabbits emerged within seven years.