New research examining COVID-19 and human sperm suggests potential risks for male infertility as well as sexual transmission.
According to researcher Dr. John Aitken, COVID-19’s pathological impact on those tested is underscored by data that shows active cases dramatically reduce testosterone to luteinizing hormones. Reduction in testosterone has a significant impact on the body’s responsiveness to Leydig cells, which stimulate the secretion of sex steroids.
Aitken said the finding is to be expected because the blood-testis barriers offer little defense against viral invasion. Pathogenic viruses such as HIV, hepatitis, mumps and HPV have been linked to testes damage that causes host infertility. The presence of the virus in the testes also leaves the host susceptible to transmitting the disease to sexual partners.
“It should be emphasized spermatozoa have a demonstrable capacity to carry viral infections from the male to the female reproductive tract,” said Aitken. “As happens during the sexual transmission of Zika, for example.” Zika virus is a mostly mosquito-borne virus that can also be sexually transmitted.
With the coronavirus, the corona-shaped spike that gives the virus its name targets ACE2 enzymes that are found in many testes cell types. Additionally, the COVID-19 virus may also gain access to male sperm cells once they leave the testes, which could be very dangerous in terms of transmission.
Mature sperm have all the equipment needed to bind and fuse with COVID-19, and then reverse transcription of viral RNA into proviral DNA. The reverse transcription produces double-stranded DNA that is integrated into the genetic material of the person. This means that human sperm can act as a vehicle for sexually-transmitted COVID-19 transmission.
A COVID-19 attack on human sperm leads to a build-up of angiotensin II, which is a hormone that regulates kidney function and blood pressure. Increased levels of this hormone cause an immune response against the invading COVID-19 virus particles that increases the availability of reactive oxygen species that causes cell death.
Prolonged exposure to elevated angiotenstin II levels can lead to cell death in sperm.
The available research suggests that when the ACE2 enzyme cleaves at specific amino acids, the exposure causes decreased sperm viability and function and can ultimately result in a loss of male fertility.