Arboviruses differ from other viruses in their need to replicate in both vertebrate and invertebrate hosts. The invertebrate is a blood-sucking arthropod that is competent to transmit the virus between susceptible animals. Arboviruses transmitted by ticks must adapt to the peculiar 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. During this phase the virus must contend with the heterophagic bloodmeal 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 indicate 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 molting by establishing an infection in at least one cell type that does not undergo histolysis. Different tick-borne viruses have different strategies for surviving the molting period, targeting a variety of tick tissues. The infection can then persist for the life span of the tick with little evidence of any detrimental effects on the tick. Transmission to a vertebrate host during feeding most probably occurs via saliva that contains virus secreted from infected salivary gland cells. The virus then enters the skin site of feeding, which has been profoundly modified by the pharmacological effects of tick saliva. At least three tick-borne viruses exploit such tick-induced host changes. This phenomenon (saliva-activated transmission) is believed to underlie "nonviremic 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 hosts. Efficient transmission of tick-borne viruses between cofeeding ticks may be a means of amplifying virus infection prevalence in F1 generations infected by transovarial transmission.

Most female ixodid ticks, once mated, feed to repletion within 6 -10 days. Previous studies indicate that an engorgement factor (EF), passed to the female during copulation, may be the stimulus for engorgement. Here, we show that extracts of the testis͞vas deferens of fed (but not unfed) male Amblyomma hebraeum contain EF bioactivity when injected into the hemocoel of feeding virgins. We have produced recombinant proteins (recproteins) from 28 feeding-induced genes in the male gonad and have identified a recombinant A. hebraeum engorgement factor (recAhEF) among these recproteins. recAhEF is a combination of two peptides, recAhEF␣ (16.1 kDa) and recAhEF␤ (11.6 kDa), neither of which has bioactivity on its own. recAhEF also stimulates salivary gland degeneration and partial development of the ovary, suggesting that it may be the same material as another male gonadal protein from this tick, male factor. We propose the name ''voraxin'' for the natural EF of ticks. When normal mated females were put on a rabbit immunized against recAhEF, 74% failed to feed beyond one-tenth the normal engorged weight within 14 days whereas all mated ticks put on a control rabbit engorged normally (mean duration of 8.8 ؎ 0.8 days). This result constitutes preliminary evidence that an anti-tick vaccine might be developed from voraxin.

Cholinomimetics (pilocarpine, carbachol, physostigmine, acetylcholine, acetyl-beta-methylcholine) and sympathomimetics (dopamine, epinephrine), when injected into the hemolymph, provoked salivary fluid secretion in the female ixodid tick Amblyomma hebraeum Koch. Atropine, but not tubocurarine or toxiferine, abolished pilocarpine-induced secretion without reducing the response to dopamine. Reserpine and guanethidine likewise selectively attenuated pilocarpine-induced secretion. Following extirpation of the synganglion, pilocarpine no longer provoked a secretory response whereas dopamine did. Thus, the salivary gland appears to be innervated directly by catecholaminergic rather than cholinergic secretory nerves. It is suggested that pilocarpine elicits salivation by interacting with muscarinic-type cholinergic receptors situated either on the cell bodies of the secretory nerves, or alternatively in the integrative or sensory pathway.

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