Basu Aabeer, Gupta Vandana, Tekade Kimaya, Prasad Nagaraj Guru
Department of Biological Sciences, Indian Institute of Science Education and Research Mohali, Sector 81, SAS Nagar, PO Manauli, Punjab, 140306, India.
Curr Res Insect Sci. 2024 Sep 27;6:100098. doi: 10.1016/j.cris.2024.100098. eCollection 2024.
Existing theories make different predictions regarding the effect of a pathogenic infection on the host capacity to reproduce. Terminal investment theory suggests that due to the increased risk of mortality, and the associated risk of losing future opportunity to reproduce, infected individuals would increase their investment towards reproduction. Life-history theory posits that due to energetic and resource costs associated with mounting an immune defense, hosts would decrease their investment towards reproduction, and reallocate resources towards defense and survival. Additionally, Somatic damage incurred by the host due to the infection is also expected to compromise the host capacity to reproduce. We explored these possibilities in females experimentally infected with pathogenic bacteria. We tested if the effect of infection on female fecundity is pathogen specific, determined by infection outcome, and variable between individual infected females. We observed that the mean, population level change in post-infection female fecundity was pathogen specific, but not correlated with mortality risk. Furthermore, infection outcome, i.e., if the infected female died or survived the infection, had no effect on fecundity at this level. At individual resolution, females that died after infection exhibited greater variation in fecundity compared to ones that survived the infection. This increased variation was bidirectional, with some females reproducing in excess while others reproducing less compared to the controls. Altogether, our results suggest that post-infection female fecundity is unlikely to be driven by risk of mortality and is probably determined by the precise physiological changes that an infected female undergoes when infected by a specific pathogen.
现有理论对致病性感染对宿主繁殖能力的影响做出了不同预测。终端投资理论表明，由于死亡风险增加以及失去未来繁殖机会的相关风险，受感染个体将增加对繁殖的投入。生活史理论假定，由于启动免疫防御会消耗能量和资源，宿主会减少对繁殖的投入，并将资源重新分配用于防御和生存。此外，宿主因感染而遭受的体细胞损伤也预计会损害其繁殖能力。我们在实验感染致病细菌的雌性动物中探究了这些可能性。我们测试了感染对雌性生育力的影响是否具有病原体特异性，是否由感染结果决定，以及在个体受感染雌性之间是否存在差异。我们观察到，感染后雌性生育力的平均群体水平变化具有病原体特异性，但与死亡风险无关。此外，感染结果，即受感染雌性是否在感染后死亡或存活，在这个水平上对生育力没有影响。在个体层面上，与感染后存活的雌性相比，感染后死亡的雌性生育力变化更大。这种增加的变化是双向的，一些雌性的繁殖量超过对照组，而另一些则低于对照组。总之，我们的结果表明，感染后雌性的生育力不太可能由死亡风险驱动，可能是由受感染雌性在感染特定病原体时所经历的精确生理变化决定的。
