ADAPTATIONS OF ARBOVIRUSES TO TICKS

Arboviruses differ from other viruses in their need to replicate in bo th vertebrate and invertebrate hosts. The invertebrate is a blood-suck ing arthropod that is competent to transmit the virus between suscepti ble animals. Arboviruses transmitted by ticks must adapt to the peculi ar physiological and behavioral characteristics of ticks, particularly with regard to blood feeding, bloodmeal digestion, and molting. Virus imbibed with the blood meal first infects cells of the midgut wall. D uring this phase the virus must contend with the heterophagic bloodmea l digestion of ticks (an intracellular process occurring within midgut cells) and overcome the as yet undefined ''gut barrier'' to infection . Genetic and molecular data for a number of tick-borne viruses indica te ways in which such viruses may have adapted to infecting ticks, but far more information is needed. After infection of midgut cells, tick -borne viruses pass to the salivary glands for transmission during the next blood-feeding episode. To do this, the virus must survive moltin g by establishing an infection in at least one cell type that does not undergo histolysis. Different tick-borne viruses have different strat egies for surviving the molting period, targeting a variety of tick ti ssues. The infection can then persist for the life span of the tick wi th little evidence of any detrimental effects on the tick. Transmissio n to a vertebrate host during feeding most probably occurs via saliva that contains virus secreted from infected salivary gland cells. The v irus then enters the skin site of feeding, which has been profoundly m odified by the pharmacological effects of tick saliva. At least three tick-borne viruses exploit such tick-induced host changes. This phenom enon (saliva-activated transmission) is believed to underlie ''nonvire mic transmission,'' whereby a virus is transmitted from an infected to an uninfected cofeeding tick through a host that has an undetectable or very low viremia. Thus tick-borne viruses that have adapted to the feeding characteristics of their tick vectors may not need to induce a virulent infection (with high viremia) in their natural vertebrate ho sts. Efficient transmission of tick-borne viruses between cofeeding ti cks may be a means of amplifying virus infection prevalence in F1 gene rations infected by transovarial transmission.