The Coinfection Of Two Morphotypes Of A Baculovirus In The Douglas-Fir Tussock Moth And The Mechanisms That Allow For This Viral Coexistence

Abstract

The Douglas-fir Tussock Moth (Orgyia pseudotsugata) is an insect species found in western United States and southern British Columbia with outbreaks occurring specifically in the Pacific Northwest, northern Rocky Mountains, California, and the Southwest. Outbreaks of the moth occur in intervals between seven and ten years and lead to the defoliation of trees, mostly the Douglas-fir (Pseudotsuga menziesii) and other Fir species, which is very detrimental to the ecosystem. To reduce and control these outbreaks, scientists have produced and spread a nuclear polyhedrosis virus that works by infecting insects, killing them, and spreading its occlusion bodies into the environment to infect more insects. However, over time, the virus has evolved to form two strains – the single-capsid nuclear polyhedrosis virus (S NPV) and the multi-capsid nuclear polyhedrosis virus (MNPV). According to scientific theories, one strain should be able to outcompete the other, sending the other strain to extinction. Yet the two strains have been able to coexist across the distributiona l range of the moth host. Thus, the goal of this paper is to understand this phenomenon in order to shed light on the dynamics of host-pathogen relationships and host-pathogen coevolution.

To understand the basic differences of the two morphotypes, we sim ply infected Douglas-fir Tussock moths with either SNPV or MNPV strains and observed the amount of time the virus took to kill the host and the number of occlusion bodies produced in the host. We discovered that, in general, the most occlusion bodies were found in infected individuals that were killed, on average, after 12 days of infection. However, when looking separately at the two morphotypes or the multiple strains, we noticed a fairly wide distribution in the amount of time it took for the insects to die. Thus, we concluded that there may be an optimal and intermediate strength of infection by the virus but that a trade-off mechanism may be the cause of this variation. This trade-off may also allow the two morphotypes, SNPV and MNPV, to coexist.