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Adene Sanchez/Getty Images It’s not the COVID-19 vaccine that will get you, say reproduction experts. It’s the virus, SARS-CoV-2, that may cause infertility. “There is evidence to suggest that infection with SARS-CoV-2 has the potential to impact both male fertility, female fertility, and certainly the health of a pregnancy of someone infected,” Dr. Jennifer Kawwass, a reproductive endocrinologist and associate professor at the Emory University School of Medicine in Atlanta told NBC News. “And there is simultaneously no evidence that the vaccine has any negative impact on male or female fertility.” Despite this striking lack of scientific evidence and the official recommendation of the Center for Disease Control and Prevention (CDC) that “all pregnant people or people who are thinking about becoming pregnant” get vaccinated, the myth persists and is a concern listed by the vaccine-hesitant. The real cause for concern is the virus, Kawwass explained, and it lies in the fact that both male and female reproductive organs contain cell receptors the virus targets. These include ACE-2, TMPRSS2, and CD147, all found in the cells of the testes, epididymis, prostate, seminal vesicles and ovarian follicles, and all known to be major SARS-CoV-2 entry factors. While the SARS-CoV-2 virus, and the disease it causes, continue to be an enigma, there is precedent for viral infections—such as the human papillomavirus (HPV), hepatitis B, hepatitis C, and HIV—being linked to infertility. SARS-CoV-2, of course, is a respiratory virus, but real-world evidence has demonstrated that its effects are not limited to the respiratory system. Recognized symptoms of long COVID—running rampant in the recovered—include fatigue, cognitive problems, shortness of breath, or racing heartbeat. Also, the high fever of 102 degrees Fahrenheit for at least three days associated with active COVID-19 has been said to cause infertility, particularly in men. “We know quite a lot about viruses, flus, and male infertility,” said reproductive urologist Dr. Paul Turek. “Seasonal flus are known to reduce male fertility … We think that it’s due to the fever associated with the illness, which overheats the testicles.” Turek went on to reassure readers that the effect was believed to be temporary. “Any infection, particularly an infection that involves fever, can affect sperm production and can affect ovulation,” said Dr. Marcelle Cedars, a reproductive endocrinologist and director of the University of California, San Francisco Center for Reproductive Health. She told NBC News that there is no evidence that COVID-19 would be different from that. While a study of 230 women of childbearing age infected with COVID-19 did not identify significant variations compared to the control group, Northwestern University Endocrinologist and Associate Professor Dr. Eve Feinberg said, “When I think about fertility, I think about what is the likelihood that a couple will take home a healthy baby. There is no question in my mind, or any scientist’s mind, that the highest likelihood of having a healthy baby during this pandemic is by getting vaccinated.”

Researchers from the Cleveland Clinic have uncovered a greater understanding of the underlying causative mechanisms responsible for cognitive impairment in patients with coronavirus disease 2019 (COVID-19), providing greater insight into an issue that has remained largely shrouded in uncertainty over the past year. The study, published online in Alzheimer’s Research & Therapy, used artificial intelligence to compare datasets comprising patients with COVID-19 and Alzheimer's disease (AD). The investigators reported no evidence suggesting SARS-CoV-2 directly infects the brain; however, there was evidence of network-based associations between the novel coronavirus and genes and proteins associated with AD and other neurologic conditions. Additionally, the investigators assessed possible relationships between COVID-19 and neuroinflammation and brain microvascular injury – two hallmarks of AD. Significant associations were found between both pathways implicated in dementia. Also, the investigators detected abnormal AD biomarker expression in cerebrospinal fluid and blood of patients who had COVID-19. Elevated expression of BSG and FURIN, two SARS-CoV-2 host factors, as well as antiviral defense genes LY6E, IFITM2, IFITM3, and IFNAR1 were observed in the brain endothelial cells of patients with AD as well as healthy controls compared with neurons and other types of cells. The researchers wrote that this finding suggests brain microvascular injury plays a potential role in COVID-19-mediated cognitive impairment. In addition, patients with APOE E4/E4, the AD risk allele, demonstrated evidence of reduced antiviral defense gene expression compared with patients who carried APOE E3/E3, indicating “a lack of expression of these genes and potentially an elevated risk of SARS-CoV-2 infection” in these patients. "We discovered that SARS-CoV-2 infection significantly altered Alzheimer's markers implicated in brain inflammation and that certain viral entry factors are highly expressed in cells in the blood-brain barrier," according to a statement made by lead study author Feixiong Cheng, PhD, an assistant staff at Cleveland Clinic's Genomic Medicine Institute. "These findings indicate that the virus may impact several genes or pathways involved in neuroinflammation and brain microvascular injury, which could lead to Alzheimer's disease-like cognitive impairment." These new research findings immediately follow other recent studies in so-called COVID-19 “long haulers,” many of whom have frequently complained of “brain fog” and other cognitive issues. In one of those studies, published in The Lancet Psychiatry, researchers found that out of 236,379 patients who had recovered from COVID-19, approximately one out of three received a diagnosis for a neuropsychiatric condition within six months. Mood disorders were the most common diagnoses. Another study in the Annals of Clinical and Translational Neurology reported that 85% of non-hospitalized patients with long COVID-19 reported at least four long-term neurologic issues. Late last year, when the ongoing pandemic still gripped the world, researchers also found that COVID-19 could age the brain and lead to cognitive decline equivalent to the brain aging by up to 10 years. The study, which included 84,000 patients from London, suggested that the infection with the novel coronavirus was linked to significant cognitive deficits for months. It remains unclear whether these cognitive deficits are transient or permanent or if vaccines could offer hope for long-haul COVID-19. "Identifying how COVID-19 and neurological problems are linked will be critical for developing effective preventive and therapeutic strategies to address the surge in neurocognitive impairments that we expect to see in the future," added Dr. Cheng.