**1. Introduction**

Virus outbreaks are largely RNA viruses whose rapid spread triggers overwhelming reduction in population and disease, following abiotic habitat stress extremes. The ability to predict a future outbreak has been significant to much research in epidemiology, many of which target statistical socioeconomics and victim genetic parameters, rather than the brutal biophysics of virus outbreak timing in its source environment. To do so requires an introduction to thermodynamics.

Virus life cycle thermodynamics are well documented [1–5] including models for the statistical mechanics and thermodynamics of virus evolution, mutations and host-infection [5, 6]. A virus always would have a stronger negative Gibbs free energy than its host in order to drive the synthesis of viral components through the hijacking of host life machinery to develop its growth products - namely virion nucleic acid, virion protein capsid and occasionally a virion lipid envelope [7]. Cross-species infection by virus are intrinsic to immunity gene instruction sharing which teaches the host how to survive abiotic stresses such as drought and frost. In this way, evolution from gene transfer and resulting changes in biodiversity are mutually interdependent. Later in this chapter we refer to this as alternate reality

#### **Figure 1.**

*Virus life cycle, adapted from Jones et al. The changing states of all viruses must be computed self-consistently over the entire virus life cycle. The figure shows three important stages of the model virus life cycle: 1. infection (entering the host cell), I*ð Þ*; 2. virus mutation-based positive host-immune by-pass* ð Þ *Ξ ; and, the successful reproduction and progeny release from the infected host cell R*ð *). Also shown are the equations for cell occupancy at each stage [5], ψ.*

formation, representing the conjoined species and habitat changes, following the stress-impetus. If so, then micro-environments may be defined as a microbial system of eco-thermodynamic symbionts which exchange nutrients mutually between them and their shared habitat [8]. The habitat might represent the microbiome of a gut system of a human. The thermodynamic balance throughout the habitat includes a maximally-sustained growth between the habitat's microbial biodiversity [6, 9]. It follows therefore, that changes to the eco-thermodynamics from abiotic and biotic stressors to the environment [9–11] results in key genetic signaling responses. These include the non-coding RNA polymerases that help species respond to disruptions to the ecothermodynamic stability. The genetic signals enable the microorganism to escape the stresses [12–16]. Species motility allows them to arrive where nutrient and moisture resources are more readily available. Virus infection and reinfection triggers resistance signaling and repair to any cellular and genetic damage [17, 18]. In so doing, the stress response can also trigger conversion of nonpathogenic bacteria and viruses into pathogenic versions. The coronavirus is also a good example of this, with mutations correlated to the stressed habitat conditions [19–21] resulting in infectious outbreaks [22]. The outbreaks help biodiversity readiness to survive. In this chapter we refer to this survival process as via thermodynamically-driven rates of virus infection and species evolution (**Figure 1**).
