Rubella virus perturbs autophagy.

Autophagy is a cellular catabolic process implicated in numerous physiological processes and pathological conditions, including infections. Viruses have evolved different strategies to modulate the autophagic process. Since the effects of rubella virus (RV) on autophagy have not yet been reported, we evaluated the autophagic activity in the Statens Seruminstitut Rabbit Cornea cell line infected with the To336 strain of RV. Our results showed that RV lowered the levels of microtubule-associated protein 1 light chain 3 B-II (LC3B-II) and the autophagy-related gene 12-autophagy-related gene 5 conjugate, inhibited the autophagic flux, suppressed the intracellular redistribution of LC3B, decreased both the average number and the size of autophagosomes per cell and impeded the formation of acidic vesicular organelles. Induction of autophagy by using rapamycin decreased both the viral yields and the apoptotic rates of infected cultures. Besides its cytoprotective effects, autophagy furnishes an important antiviral mechanism, inhibition of which may reorchestrate intracellular environment so as to better serve the unique requirements of RV replication. Together, our observations suggest that RV utilizes a totally different strategy to cope with autophagy than that evolved by other positive-stranded RNA viruses, and there is considerable heterogeneity among the members of the Togaviridae family in terms of their effects on the cellular autophagic cascade.

Mate-guarding success depends on male investment in a butterfly.

Males of many insects, including butterflies, produce mate-guarding devices, such as mating plugs, to prolong guarding and prevent future female matings in the male's absence. In a few butterflies, large external mate-guarding devices, that is, sphragides, occur. Gór et al. (Behaviour, 160, 2023 and 515-557) found conspicuously large size and morphological variation of mate-guarding devices within a single population of the potentially polyandrous Clouded Apollo (Parnassius mnemosyne, L.) butterfly. They termed the externally visible male-produced devices as Copulatory opening APpendices (CAP) consisting of small devices, termed small CAPs and the much larger shield (i.e. sphragis). Our aim was to reveal CAP replacement dynamics within females during their lifetime and to understand how male investment into small CAPs or shields was (i) related to CAP persistence on the female, that is securing paternity, (ii) associated with female quality, measured as size and (iii) with actual adult sex ratio. We investigated a univoltine Clouded Apollo population to estimate CAP replacement risks, using multistate survival models, in an extensive observational study through 6 years based on mark-recapture. Shields were the most frequent mate-guarding devices and were more persistent than small CAPs, often lasting for life, excluding future matings. Thus, most females bearing a shield were deprived of postcopulatory female choice, and the genetic variance in their offspring could be reduced compared to those bearing small CAPs, thus mating more often. The ratio of shields to all CAPs gradually decreased towards the end of the flight period. Males were more prone to produce a shield when mating females with wider thoraces and when the ratio of males (i.e. competition) was higher in the population. To our best knowledge, this is the first quantitative study to investigate potential factors on which male investment in mate-guarding devices may depend, and how the variation in these devices impacts CAP persistence on females.

Phenotypic senescence in a natural insect population.

Senescence seems to be universal in living organisms and plays a major role in life-history strategies. Phenotypic senescence, the decline of body condition and/or performance with age, is a largely understudied component of senescence in natural insect populations, although it would be important to understand how and why insects age under natural conditions. We aimed (i) to investigate how body mass and thorax width change with age in a natural population of the univoltine Clouded Apollo butterfly (Parnassius mnemosyne, Lepidoptera: Papilionidae) and (ii) to assess the relationship of this change with sex and wing length. We studied a population between 2014 and 2020 using mark-recapture during the whole flight period each year. Repeated measurements of body mass and thorax width and single measurements of wing length were performed on marked individuals. We analyzed body mass and thorax width change with age (days since marking), wing length, and the date of the first capture. Both body mass and thorax width declined nonlinearly with age. Individuals appearing earlier in the flight period had significantly higher initial body mass and thorax width and their body mass declined faster than later ones. Initial body sizes of females were higher, but males' body sizes decreased slower. Initial thorax width showed higher annual variation than body mass. To our best knowledge, this is the first study that revealed phenotypic senescence in a natural butterfly population, using in vivo measurements. We found sexual differences in the rate of phenotypic senescence. Despite the annual variation of initial body sizes, the rate of senescence did not vary considerably across the years.

Herpes simplex virus types 1 and 2 modulate autophagy in SIRC corneal cells.

Autophagy and apoptosis function as important early cellular defense mechanisms in infections and other diseases. The outcome of an infection is determined by a complex interplay between the pathogenic microorganism and these intracellular pathways. To better understand the cytopathogenicity of Herpes simplex virus types 1 and 2 (HSV-1 and - 2), we studied the effect of these viruses on the autophagic and apoptotic processes in the SIRC corneal cell line. Infection with the KOS strain of HSV-1 and a wild-type strain of HSV-2 enhanced autophagosome formation, triggered cytoplasmic acidification, increased LC3B lipidation and elevated the ratio of apoptotic cells. The autophagy inhibitor bafilomycin A1 triggered a significant increase in the apoptotic responses of HSV-1 and HSV-2-infected cells. Thus, both HSV types affect autophagy and apoptosis in a coordinated fashion, and autophagy plays cytoprotective role in HSV-infected cells via antagonizing apoptosis. Together these data implicate autophagy in the pathogenic mechanism of herpetic keratitis.