Scientists have identified a sexually-transmitted virus that makes male and female crickets functionally sterile -- then it encourages sexual encounters, and keeps them wanting more. Researchers call it a “viral aphrodisiac,” but really, IIV-6/CrIV is just plain messed up.
When their Gryllus texensis crickets stopped laying eggs, a Dalhousie University team led by Shelley Adamo used an electron microscope and PCR analysis to reveal a virus attacking their “fat bodies,” an important organ for protein production, immune function, and lipid storage. By this point, the organ had become blue and swollen.
Turns out, during the infection, the fat body hypertrophies (or gets bigger, the opposite of atrophies). At the same time, egg production withers, leaving the oviducts empty of eggs and making the females effectively sterile. An examination of infected males suggests that the testis is not invaded by the virus, however sperm taken from the spermatophore (the capsule containing the sperm) of infected males showed little or no motility.
Sperm that can’t swim, oviducts without eggs. This “parasitic castration” means the virus gets more of its host’s resources -- since reproduction is a huge energy expenditure -- but without actually killing it.
And here’s worst part: The males and females continued to mate when infected. In fact, the virus somehow changes their behavior, making the infected males even quicker to court females than uninfected males. When paired with females, healthy (control) males waited about 10 minutes before they started their courtship rituals. Males sick with a bacterial infection took about 13 minutes. Males infected with IIV-6/CrIV got it on in 3. About half of the pairings between infected males and uninfected females resulted in transmission.
The virus encourages this continued sexual behavior of its host because it increases transmission. Not only that, but the typical loss in appetite and reduction of sexual behavior -- normal things induced by the immune system of sick animals -- are completely absent in infected crickets. Their lymph (called hemolymph) and enzyme activity suggests a reduction in immune protein production by the fat body. During IIV-6/CrIV infection, the immune signals that induce “sickness behaviors” are absent -- because curtailing those under-the-weather feelings increases sexual encounters, which spreads the pathogen to more uninfected bugs. Parasitic mind control. Brilliant, and nasty.
The work was published in the Journal of Experimental Biology last month.
[Via National Geographic, The Week]
Image: T. J. Walker, University of Florida
