Biological impact of Galactic Cosmic Rays [GCRs]
The biological impact of GCRs is primarily governed by their high linear energy transfer (LET) and high ionizing potential, characterized by dense energy deposition along the tracks of the charged particles as they traverse biological matter [17, 18]. Unlike low-LET radiation such as X-rays or gamma rays, GCRs and particularly heavy ions with high charge and energy (HZE) like carbon atoms (C), oxygen (O), neon(Ne), silicon (Si), calcium (Ca), and iron (Fe) can produce dense ionization columns that induce complex, clustered genetic lesions that are difficult for cellular mechanisms to repair [18, 19]. When primary GCRs interact with the Earth’s atmosphere, they undergo nuclear spallation. This process generates secondary particle cascades, including neutrons, protons, pions, and muons [19]. Neutrons, despite being uncharged, possess high Relative Biological Effectiveness (RBE) (Fig. 1B). Because they are highly penetrating, they frequently collide with hydrogen nuclei in biological tissue, producing recoil protons that can cause localized, high-density damage [19–21]. These secondary cascades can penetrate the troposphere, contributing to a continuous background of ionizing radiation that fluctuates with solar activities and Earth atmospheric conditions [22, 23].
The resulting genetic damage may occur via two primary pathways, in which high-energy particles directly strike DNA, causing double-strand breaks (DSBs) and locally multiply damaged sites (LMDS) [19,24]. The radiation can induce the radiolysis of water molecules, generating reactive oxygen species(ROS) such as hydroxyl radicals (⋅OH). These radicals cause oxidative base modifications and systemic oxidative stress [19]. In the context of viral dynamics, GCR-induced mutagenic pressure may alter viral quasispecies structure. At moderate levels, such mutational stress could enhance viral diversification, potentially facilitating reactivation or amplification. However, if the mutation rate exceeds the error threshold, viral populations may enter an error-catastrophe regime [24].
Furthermore, GCRs flux is modulated by solar cycle and the Hale Cycle. During solar minima, the weakened HMF allows for increased GCRs penetration into the inner solar system [16]. These periods of elevated GCRs flux, particularly during specific solar magnetic polarities (A < 0 or A > 0), have been hypothesized to act as external mutagenic drivers that may promote abrupt viral genetic shifts, potentially enhancing viral virulence or facilitating zoonotic spillover events [25, 26]. In host populations, chronic exposure to GCR induced secondary radiation can theoretically lead to altered immune responsiveness, potentially compromising the host’s ability to clear emerging viral variants [19, 27–30].
