13 Role of Reverse Transcriptase in Retroviral Recombination

Abstract

Retroviruses replicate with frequent errors that result in mutations. Frequent recombination allows distribution of these mutations in the population, increases the variation in the population, and removes lethal mutations. These features are dramatically demonstrated in recent studies of human immunodeficiency virus type-1 (HIV-1) sequences (Vartanian et al. 1991). Frequent recombination has long been known to be a common feature of retroviruses (Vogt 1971; Kawai and Hanafusa 1972). Both simpler oncoretroviruses and more complex lentiviruses recombine frequently (Clavel et al. 1989). Two features of retroviral recombination are always reported: (1) Recombination occurs at very high frequencies; it is common to observe 10–25% recombination (Vogt 1971; Kawai and Hanafusa 1972; Blair 1977). (2) Multiple crossover events are observed; markers as close as 1 kb apart are reported to segregate independently (Coffin 1979).

Recombination is most often observed between exogenous retroviruses, but it is not limited to them. Recombination can also occur between endogenous and exogenous viruses (for review, see Eisenman et al. 1980; Linial and Blair 1982; Stoye and Coffin 1985). Retroviruses can also transduce host sequences at a low frequency (for review, see Bishop and Varmus 1985), presumably through a process involving nonhomologous recombination.

Both homologous recombination and nonhomologous recombination are discussed in this chapter. Earlier work has been summarized in many excellent reviews (Hunter 1978; Coffin 1979; Linial and Blair 1982; Bishop 1983; Skalka et al. 1983; Bishop and Varmus 1985; Katz and Skalka 1990). We emphasize here the present knowledge of the mechanisms of recombination.

HOMOLOGOUS RECOMBINATION
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