Semen as virus reservoir?


The recent Ebola outbreak prompted our group to perform a systematic literature search about semen and the Ebola virus. Of interest was the fact that the Ebola virus has been cultured from semen samples collected 2 and 3 months after disease onset, despite that the virus was cleared from the blood of these patients [1–3]. Based on this information, we advocate the evident need to avoid unprotected sexual intercourse for at least 3 months after clearance of the Ebola virus from the blood [4]. More recently, NEJM published two interesting papers regarding the Ebola virus and semen. In the first paper, the authors found that semen samples from Ebola virus disease (EVD) survivors remained positive for up to 9 months (272 days) after the onset of symptoms. However, the detection was done by quantitative RT-PCR, thereby indicating the presence of the virus but not whether it is infectious [5]. The second article is based on a case report regarding a 44-year-old woman infected with the Ebola virus after unprotected vaginal intercourse with a male survivor of EVD [6]. This persistence of the Ebola virus (and declining persistence with increasing months) since the onset of EVD is a proof that semen can act as an Ebola virus reservoir. Similarly, Foy et al. reported in 2011 that the Zika virus (family: Flaviviridae, genus: Flavivirus), a mosquito-borne arbovirus, was transferred directly from person-to-person (husband to wife, Colorado, USA). This most probably occurred through sexual intercourse in the days after the husband was infected during a trip to Senegal but before the onset of his clinical illness [7]. A further case of sexual transmission was reported in Texas early in 2016 when a traveler returning from Venezuela’s sexual partner also became infected [8]. Likewise to the Ebola findings, semen samples tested positive for the Zika virus even though it came up negative in blood [9]. In addition, human immunodeficiency virus (HIV) shedding was shown to persist in semen [10, 11 and revised in 12] from individuals receiving suppressive highly active antiretroviral therapy, thereby indicating that the male genital tract may be acting as a constitutive viral reservoir. Likewise, HIV transfer by spermatozoa into the oocyte [13] or macrophages [14] has been shown, indicating at least that spermatozoa can act as vectors of HIV constituting a potential source of infection during intercourse. In vitro results from our studies show the presence of viral RNA, but not DNA, in sperm samples from HIV-1-negative individuals, after in vitro exposure to HIV particles. These findings suggest an interaction between HIV and spermatozoa [15, 16] whereby the virus use cellular receptors such as the mannose receptor [15, 17] and the heparin sulfate proteoglycan endocytosis receptor [18, 19] for entry into the cell. Additionally, previous detection of proviral DNA in spermatozoa from HIV-infected men has also been shown [13, 20–22]. The notion of semen as a virus reservoir begs several concerns [23]. These include the possible testing of semen as a more accurate screening method for viral infections, establishing the time for clearance of viral particles from the semen * Walter D. Cardona Maya

DOI: 10.1007/s10815-016-0747-8

Cite this paper

@article{Maya2016SemenAV, title={Semen as virus reservoir?}, author={Walter D. Cardona Maya and S. du Plessis and P A Velilla}, journal={Journal of Assisted Reproduction and Genetics}, year={2016}, volume={33}, pages={1255-1256} }