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Review  |  Open Access  |  29 May 2023

The Neural correlates of COVID-19-induced erectile dysfunction in males

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Ageing Neur Dis 2023;3:8.
10.20517/and.2023.09 |  © The Author(s) 2023.
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Emerging evidence suggests that there are long-term complications after recovery from COVID-19, which involve multiple systems and lead to deterioration of the quality of life. Among these different complications, male sexual dysfunction, in particular erectile dysfunction, is one of the complications being identified recently. It was initially hypothesized that due to the presence of Angiotensin-converting enzyme II (ACE2) and transmembrane protease serine 2 (TMPRSS 2) in testes and Leydig cells, the male reproductive system is vulnerable to the infection of COVID-19, which may lead to a decrease in testosterone production and sexual dysfunction. However, evidence from a recent neurological study suggests that COVID-19 may be directly associated with dysregulation of the nervous systems at the central level in regions including the limbic system (e.g., hippocampus and amygdala), hypothalamus, brainstem, and the peripheral system (e.g., sympathetic nerves, olfactory bulb). As these affected regions are crucial for sexual behaviors, these observations may provide an alternate explanation for sexual dysfunction in COVID-19 survivors. To explore the potential involvement of the nervous system in sexual dysfunction induced by COVID-19, this review discusses the recent findings from the neurological perspective and states the possible research work that may be needed to delineate the underlying pathology.


COVID-19, long COVID, sexual dysfunction, central nervous system, male reproductive system


Since late 2019, the outbreak of coronavirus disease 2019 (COVID-19) has been a major health concern. Caused by a novel form of coronavirus termed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), multiple organs and tissues expressing the angiotensin-converting enzyme 2 (ACE2, a major receptor for SARS-CoV-2[1]) and the transmembrane protease serine 2 (TMPRSS2), which facilitates the fusion of the virus and cellular membranes[2]) are susceptible to coronavirus infection. ACE2 and TMPRSS2 are abundantly expressed in the respiratory system (e.g., nasal cavity), digestive system (e.g., esophagus, small intestine, large intestine, gall bladder), reproductive system (e.g., fallopian tube, testis), nervous system at central and peripheral level (e.g., cortex, substantia nigra, olfactory mucosa) , and other distinctive organs (e.g., heart, kidney[3,4]). The abundance of ACE2 and TMPRSS2 expression implies the relatively high risk of being susceptible to the infection of aSARS-CoV-2. Concurring with the expression level of ACE2 and RMPRSS2, signs and symptoms of COVID-19 are usually tied to the abovementioned organs, including respiratory (e.g., cough, and sore throat), gastrointestinal (e.g., diarrhea), olfactory (e.g., anosmia and ageusia) and neurological symptoms (e.g., headache and pain[5]). Due to the high expression level of ACE2 and SARS-CoV-2 in reproductive organs, it has been hypothesized that the reproductive function would also be affected by the COVID-19 infection. Testosterone, the male sex hormone produced by Leydig cells in the testis, was speculated to facilitate COVID-19 entry into testicular cells by augmenting the expression of ACE2 and TRMPRSS2[6]. The presence of COVID-19, in turn, damages the testis, induces hypogonadism, causes vascular damage in the penis, and ultimately leads to erectile dysfunction[7]. Since dysfunction of the reproductive system may not be the primary complaint of patients and not easy to observe in clinical situation, sexual dysfunction due to COVID-19 may be mainly reported by patients after recovery from the disease.


The aetiology of sexual dysfunction can have central or peripheral origins. Central causes of sexual dysfunction, such as erectile dysfunction, are common among individuals with spinal cord injury[8]. Additionally, peripheral sexual dysfunction can occur as a result of factors affecting the peripheral nervous system[9]. The neurological effects of COVID-19 at central and peripheral nervous system level may have negative implications for sexual function[10]. Presentations of central nervous system alterations caused by COVID-19 include dizziness, headache, impaired consciousness, acute cerebrovascular disease, ataxia, and seizures, while peripheral nervous system manifestations include anosmia, dysgeusia, and nerve pain[11]. Neuronal damage detected in brain regions vulnerable to hypoxia, such as the neocortex, hippocampus, and cerebellum, has been observed in autopsies of COVID-19 patients[12], and alterations in certain areas of the brain such as the hippocampus, that is involved in sexual arousal, could also impact the erectile response[12,13]. On the other hand, reports of neurological complaints after recovering from COVID-19 point out the involvement of the peripheral nervous system[14]. For instance, disruption of the sensory nerves responsible for sending the local sensory signals to the brain can lead to erectile dysfunction[9]. Furthermore, fatigue associated with symptoms such as cardiovagal function, postural hypotension, tachycardia, and bladder, bowel and sexual dysfunction suggests the role of dysfunctional autonomic system responses associated with COVID-19[14], and autonomic dysfunction has been identified as an important factor in erectile dysfunction[15].

The earliest concerns about COVID-19-associated sexual dysfunction can be traced back to mid-2020[16]. It was reported that the presence of orchitis and inflammation of testicles was found in about 20% of males with COVID-19 due to primary coronavirus infection or a secondary autoimmune response and testicular pain was a possible symptom in COVID-19 patients[17]. Subsequent case reports presented COVID-19 patients who experienced sexual dysfunction, including anorgasmia after recovery from COVID-19[18], Peyronie’s disease with endothelial dysfunction[19], erectile dysfunction, and premature ejaculation[20]. As COVID-19 viral particles were found in testicular samples (but not in semen) and impaired spermatogenic function was shown in COVID-19 patients[21,22], these findings provide evidence to support the direct infection of testicular tissue by the coronavirus and the impact on the male reproductive function.

Later, studies on the prevalence of erectile dysfunction among COVID-19 patients provided further evidence to show the association between COVID-19 and erectile dysfunction. A study conducted by Sansone et al. (2021) found those patients infected by SARS-CoV-2 had a higher risk of developing erectile dysfunction[23]. Since the association observed did not imply any causal relationship, it is unclear whether COVID-19 causes erectile dysfunction or whether other underlying factors (e.g., age, ethnicity, and socioeconomic status) increase the risk of erectile dysfunction and COVID-19 simultaneously[24]. Other studies found similar findings. For instance, studies on COVID-19 recovery showed that erectile dysfunction was likely to be transient in subjects who recovered from COVID-19[25,26]. Estimations showed that the odds ratio of erectile dysfunction in COVID-19 patients was 3.3 times higher than in non-COVID-19 patients[27].

It was hypothesized that the male sexual dysfunction associated with COVID-19 was caused by several factors[28]. (1) Endothelial dysregulation: Since ACE2 and TMPRSS2 are abundantly expressed on the endothelial cell surface, COVID-19 may enter the endothelial cells in the penile tissue leading to endothelial dysfunction and subsequently affecting erection. (2) Hypogonadism: The infection of Leydig and Sertoli cells in the testis may disrupt the production of testosterone, which contributes to erectile dysfunction. (3) Psychosocial stress: Fear of transmission, awareness of social distancing, social isolation, and quarantine result in psychosocial stress, which would be another contributor to sexual distress and dysfunction. (4) Pulmonary impairment: A decrease in physical fitness due to pulmonary impairment may also affect sexual activity[29]. (5) Spinal cord damage: Spinal cord dysfunction due to spinal cord ischemia, epidural abscess, or demyelination has been observed in individuals after COVID-19 infection[30,31]. (6) Peripheral nerve damage: Dysfunctional autonomic system responses and aberrant sensory function associated with COVID-19 infection[11,14].

Although the reproductive damages of COVID-19 infection are still unclear, the presence of COVID-19 in the reproductive system (e.g., testis, which show high expression of ACE2) and the neuroinflammatory response indicate the impact of COVID-19 infection on sexual function[32,33]. Most male patients infected with COVID-19 present a cytokine storm that may lead to immune-mediated organ damage[33,34]. In other disorders, cytokines are known to pass the blood-brain barrier triggering a cytokine storm in the nervous system[32]. The cytokine storm (e.g., IL6, IL2R, IL10, TNFα, and MCP-2) can create dysfunction in different regions of the brain, including those responsible for the regulation of sexual functions (e.g., hippocampus and cerebellum) and lead to manifestations of neurological symptoms[12,32]. Central nervous system inflammatory lesions in COVID-19 patients have been previously reported suggesting the damage observed may be mediated by the cytokine storm[35,36]. The central nervous system to COVID-19-mediated lesions is more susceptible due to the increased vulnerability to hypoxia and a higher expression of ACE2 compared to the peripheral nervous system[32]. However, the peripheral nervous system is also affected. For instance, in peripheral nerves, COVID-19 spikes interact with GM1gangluoside leading to cross-reactivity and production of antibodies against the antigens; this response induces peripheral nerve damage, which may lead to erectile dysfunction[37,38]. An elevated level of pro-inflammatory cytokines, including interleukin-6, may indicate a higher risk of developing erectile dysfunction[39]. As cytokine storm is a hallmark of COVID-19, infection severity would also serve as a predictor of erectile dysfunction[40]. Other predictors or post-COVID-19-related erectile dysfunction factors include but are not limited to age over 40 years and diagnosis of depression[41].


The impact of the COVID-19 pandemic is not only on those who contracted SARS-CoV-2 but also on people with no COVID-19 infection[42]. During the epidemic, deteriorated sexual functioning including erectile dysfunction, diminished ejaculation control ability, and decreased sexual satisfaction were observed in people who were not infected by COVID-19[43]. Increased anxiety and depression are implicated in the sexual issues observed in people without COVID-19[43,44]. The increase in the prevalence of erectile dysfunction may be indirectly reflected by the increase in sales of and interest in phosphodiesterase-5 inhibitors, which are common erectile dysfunction medications[45,46]. In a study on admission to urology clinics, the number of patients with erectile dysfunction and varicocele increased significantly during the pandemic, and psychogenic factors rather than viral infection were underlying causes of sexual dysfunction in people without COVID-19 infection[47]. Erectile dysfunction was also reported in healthcare professionals working in COVID-19 settings due to the stressful working environment that affected their psychological well-being[48]. It is important to acknowledge that the incidence of depression and anxiety in COVID-19 patients is notably higher than in those without the infection[49,50]. As a result, it is reasonable to hypothesize that depression and anxiety may contribute to sexual dysfunction in COVID-19 patients as well. The heightened psychological distress experienced by this population, in conjunction with the direct and indirect effects of the virus, may amplify the risk of developing sexual dysfunction.

Unlike patients infected with COVID-19, the impact of the pandemic on the sexual functions of uninfected individuals is likely due to psychosocial factors including stress, concerns about virus transmission and social distancing as well as personality traits, which are not directly related to factors associated with sexual dysfunction in COVID-19 patients[51,52]. Evidence from cross-sectional studies showed that during the pandemic, sexual desire and sexual activity were suppressed due to social distancing concerns, and sexual activities that can be carried out by isolated individuals (e.g., pornography consumption) were increased[53-55].


Though most of the current perspectives on COVID-19-induced sexual dysfunctions focus on direct infection of the reproductive tissues with SARS-CoV-2, it is highly plausible that the dysfunction is not only caused by the dysfunction of the reproductive system but also by alterations in the central nervous system. For instance, erection is a spinal reflex in which penile tissues (e.g., corpora cavernosa), the autonomic nervous system, and cortical tissues participate[56]. Apart from the reflex arc at the spinal level, sensory information including visual, tactile, and olfactory stimulation and sexual imagination, which are processed by the cortex, are important in supraspinal control of erection[56]. Since ACE2 and TMPRSS2 are expressed in relatively high abundance in different regions of the brain, including the olfactory bulb, cerebral cortex, striatum, hypothalamus, hippocampus, and brainstem[57-60], COVID-19 infection in these cortical and subcortical regions may interfere with the supraspinal control of penile erection[61]. In the following section, the role of these cortical/subcortical regions involved in sexual functioning is discussed, as well as the possibility of their contribution to COVID-19-induced sexual dysfunction.

Medial preoptic area of the hypothalamus

Medial preoptic area (MPOA) is a key region that regulates sexual behaviour[62]. This region receives input from the olfactory system via the bed nucleus of the stria terminalis, amygdala, and hippocampus[63]. When the MPOA was lesioned, substantial, long-term suppression of sexual behavior, including fewer mounts, intromissions and ejaculations, was observed[64]. On the other hand, stimulation of the MPOA promoted penile erection[65]. The MPOA is suggested to integrate hormonal and sensory signals for sexual behavior, process relevant information and redistribute this information to downstream structures like the paraventricular nucleus and caudal spinal cord nuclei, which control erections[66]. As the hypothalamus expresses ACE2 and TMPRSS2, it is also a potential target for SARS-CoV-2, which may invade different hypothalamic circuits of the olfactory system. The coronavirus may be transmitted trans-synaptically and ultimately spread to interconnected brain regions[67].

Paraventricular nucleus of the hypothalamus

The paraventricular nucleus (PVN) receives projection from the MPOA and is an important supraspinal control center of erection[66]. PVN contains premotor neurons that project directly to the caudal spinal cord, which in turn contains neurons connected to the corpus carvernosum[66]. Stimulation of the PVN by different agonists including oxytocin and glutamate elicits penile erection[68], while a lesion of this region leads to fewer noncontact erection and increased latency to erection[69]. As a supraspinal erectile control center, PVN is another vulnerable area susceptible to COVID-19 infection due to the high expression of ACE2 in this region[70]. Interestingly, the infection of the PVN may be expected to affect the physiological status leading to fatigue, anxiety and changes in the circadian rhythm[71,72]. However, there is still a lack of studies on the connection between PVN and sexual dysfunction in the context of COVID-19.


The thalamus has been traditionally regarded as a sensory gateway to higher cortical regions, which relay sensory information, apart from chemosensation, to the cortex[73]. Similar to other sensory modules, the sexual stimuli from peripheral nerves of the penis are relayed by the thalamus and sent to higher cortical regions[74]. Deep brain stimulation of the thalamus was shown to influence penile erection[75]. Due to the complex interaction with the cortex and other subcortical regions, the involvement of the thalamus in sexual functioning can be observed in multiple aspects. The thalamus expresses high levels of ACE2[76]. Therefore, the thalamus may be another possible affected site by the coronavirus.


The amygdala has a widespread connection with other cortical and subcortical regions, and it has a close connection with the olfactory system and also sexual functions[77]. It is involved in the processing of olfactory and pheromonal signals which are transmitted from the olfactory bulb and the olfactory tract[74]. Through the integration of various stimuli, the amygdala regulates social, emotional and sexual functions. For instance, stimulation of the amygdala evokes orgasm-like sensations[78]. Disruptions in this region may induce functional impairment at different levels, including emotional functions, sexual functions, and resilience to stress. Thus, potential neuroinvasion into the amygdala may affect sexual functioning from the psychosocial/stress aspect to neural pathways associated with sexual function. Though ACE2 and TMPRSS2 expression is not particularly high in the amygdala, its close connection with the olfactory system may render vulnerability to this area through trans-synaptic transmission.


A proportion of COVID-19 patients may develop post-acute COVID Syndrome (Long COVID). Sexual dysfunction has been proposed as a possible characteristic of Long COVID[79], which could have a significant impact on the quality of life for patients after recovery. While the pathophysiology underlying COVID-19-induced sexual dysfunction remains unclear, it is essential to consider various factors that may contribute to this condition. Recent findings suggest the potential for neuroinvasion by the virus[80], but it is crucial to examine traditional sources of erectile dysfunction (ED) alongside COVID-19-related factors. This review acknowledges the need for further research to establish a strong link between CNS-induced ED, COVID-19, and Long COVID.

Research to understand the impact and mechanism of long COVID on sexual dysfunction is still limited. Critical questions in this field include: What neural mechanisms can be targeted to restore sexual function after COVID-19? How do the neural correlates of COVID-19-induced sexual dysfunction associate with other physiological mechanisms relevant to sexual function? How do neural correlates affect the long-term prognosis of sexual dysfunction associated with long COVID? Therefore, further studies are needed to delineate the causal relationship between COVID-19 and sexual dysfunction to identify targets for treatment to improve the quality of life of the patients. Considering these conditions, it becomes essential to rigorously examine conventional etiological factors associated with erectile dysfunction in parallel with investigating the potential connection between Long COVID and sexual dysfunction. This integrative research approach will enable a deeper comprehension of the pathophysiological underpinnings of COVID-19-related sexual dysfunction and clarify its potential contribution to Long COVID. Ultimately, the insights gained from these investigations will facilitate the development of targeted and effective therapeutic interventions to address this significant clinical concern.


Author’s contribution

Study conception and design: Lau BWM, Lee JCD, So KF

Literature search and review: Lau BWM, Sanchez-Vidaña DI, Chan JNM

Draft manuscript and preparation: Lau BWM, Lee JCD, Sanchez-Vidaña DI, Chan JNM

Review and revision of paper: Lau BWM, Lee JCD, Sanchez-Vidaña DI, Chan JNM, Lau WKW, So KF

Approval of final version: Lau BWM, Lee JCD, Sanchez-Vidaña DI, Chan JNM, Lau WKW, So KF

Availability of data and materials

Not applicable.

Financial support and sponsorship

This manuscript is supported by GRF to BWM Lau, Reference No. 15105621 and HMRF, COVID1903007.

Conflicts of interest

The authors declare that they have no conflicts of interest regarding the publication of this manuscript. All authors have read and approved the final version of the manuscript.

Ethical approval and consent to participate

Not applicable.

Consent for publication

Not applicable.


© The Author(s) 2023.


1. Dong M, Zhang J, Ma X, et al. ACE2, TMPRSS2 distribution and extrapulmonary organ injury in patients with COVID-19. Biomed Pharmacother 2020;131:110678.

2. Navarra A, Albani E, Castellano S, Arruzzolo L, Levi-Setti PE. Coronavirus disease-19 infection: implications on male fertility and reproduction. Front Physiol 2020;11:574761.

3. Lechien JR, Radulesco T, Calvo-Henriquez C, et al. ACE2 & TMPRSS2 expressions in head & neck tissues: a systematic review. Head Neck Pathol 2021;15:225-35.

4. Qi J, Zhou Y, Hua J, et al. The scRNA-seq expression profiling of the receptor ace2 and thecellular protease tmprss2 reveals human organs susceptible to sars-cov-2 infection. Int J Environ Res Public Health 2021;18:284.

5. Struyf T, Deeks JJ, Dinnes J, et al. Cochrane COVID-19 Diagnostic Test Accuracy Group. Signs and symptoms to determine if a patient presenting in primary care or hospital outpatient settings has COVID-19. Cochrane Database Syst Rev 2022;5:CD013665.

6. Lisco G, Giagulli VA, De Pergola G, De Tullio A, Guastamacchia E, Triggiani V. Covid-19 in man: a very dangerous affair. Endocr Metab Immune Disord Drug Targets 2021;21:1544-54.

7. Sansone A, Mollaioli D, Ciocca G, et al. Addressing male sexual and reproductive health in the wake of COVID-19 outbreak. J Endocrinol Invest 2021;44:223-31.

8. Krassioukov A, Elliott S. Neural control and physiology of sexual function: effect of spinal cord injury. Top Spinal Cord Inj Rehabi ;23:1-10.

9. Calabrò RS, Gervasi G, Naro A, de Luca R, Marullo M, Bramanti P. Erectile dysfunction in individuals with neurologic disability: a hospital-based cross-sectional study. Innov Clin Neurosci 2016;13:10-4. Available from: PMC4896824/[Last accessed on 24 May 2023].

10. Hsieh TC, Edwards NC, Bhattacharyya SK, Nitschelm KD, Burnett AL. The epidemic of covid-19-related erectile dysfunction: a scoping review and health care perspective. Sex Med Rev 2022;10:286-310.

11. Mao L, Jin H, Wang M, et al. neurologic manifestations of hospitalized patients with coronavirus disease 2019 in wuhan, china. JAMA Neurol 2020;77:683-90.

12. Iadecola C, Anrather J, Kamel H. Effects of COVID-19 on the nervous system.

13. Burnett AL. Neurophysiology of erectile function: androgenic effects. J Androl 2003;24:S2-5.

14. Taga A, Lauria G. COVID-19 and the peripheral nervous system. J Peripher Nerv Syst 2022;27:4-30.

15. Pop-Busui R, Hotaling J, Braffett BH, et al. DCCT/EDIC Research Group.

16. José FG, González JGÁ, Molina JMC, et al. [SARS-CoV-2 infection: implications for sexual and reproductive health. Rev Int Androl 2020;18:117-23.

17. Marca A, Busani S, Donno V, Guaraldi G, Ligabue G, Girardis M. Testicular pain as an unusual presentation of COVID-19: a brief review of SARS-CoV-2 and the testis. Reprod Biomed Online 2020;41:903-6.

18. Shoar S, Khavandi S, Tabibzadeh E, et al. A late COVID-19 complication: male sexual dysfunction. Prehosp Disaster Med 2020;35:688-9.

19. Rainer Q, Molina M, Ibrahim E, Saltzman R, Masterson T, Ramasamy R. Peyronie's disease in a patient after COVID-19 infection: a case report. Andrologia 2021;53:e14219.

20. Salama N, Blgozah S. COVID-19 and male sexual functioning: a report of 3 recovered cases and literature review. Clin Med Insights Case Rep 2021;14:11795476211020593.

21. He Y, Wang J, Ren J, Zhao Y, Chen J, Chen X. Effect of COVID-19 on male reproductive system - a systematic review. Front Endocrinol (Lausanne) 2021;12:677701.

22. Aksak T, Satar DA, Bağci R, Gülteki N EO, Coşkun A, Demi Rdelen U. Investigation of the effect of COVID-19 on sperm count, motility, and morphology. J Med Virol 2022;94:5201-5.

23. Sansone A, Mollaioli D, Ciocca G, et al. "Mask up to keep it up": preliminary evidence of the association between erectile dysfunction and COVID-19. Andrology 2021;9:1053-9.

24. Rozenfeld Y, Beam J, Maier H, et al. A model of disparities: risk factors associated with COVID-19 infection. Int J Equity Health 2020;19:126.

25. Hu B, Ruan Y, Liu K, et al. A mid-to-long term comprehensive evaluation of psychological distress and erectile function in COVID-19 recovered patients. J Sex Med 2021;18:1863-71.

26. Karkin K, Alma E. Erectile dysfunction and testosterone levels prior to COVID-19 disease: what is the relationship? Arch Ital Urol Androl 2021;93:460-4.

27. Katz J, Yue S, Xue W, Gao H. Increased odds ratio for erectile dysfunction in COVID-19 patients. J Endocrinol Invest 2022;45:859-64.

28. Kaynar M, Gomes ALQ, Sokolakis I, Gül M. Tip of the iceberg: erectile dysfunction and COVID-19. Int J Impot Res 2022;34:152-7.

29. Malik J, Younus F, Iftikhar I, Usman M. Love in the time of COVID-19: a scoping review on male sexual health. J Community Hosp Intern Med Perspect 2021;11:496-500.

30. Mondal R, Deb S, Shome G, Ganguly U, Lahiri D, Benito-León J. COVID-19 and emerging spinal cord complications: a systematic review. Mult Scler Relat Disord 2021;51:102917.

31. Sampogna G, Tessitore N, Bianconi T, et al. Spinal cord dysfunction after COVID-19 infection. Spinal Cord Ser Cases 2020;6:92.

32. Guerrero JI, Barragán LA, Martínez JD, et al. Central and peripheral nervous system involvement by COVID-19: a systematic review of the pathophysiology, clinical manifestations, neuropathology, neuroimaging, electrophysiology, and cerebrospinal fluid findings. BMC Infect Dis 2021;21:515.

33. Kharbach Y, Khallouk A. Male genital damage in COVID-19 patients: are available data relevant? Asian J Urol 2021;8:324-6.

34. Wang Y, Wang Y, Chen Y, Qin Q. Unique epidemiological and clinical features of the emerging 2019 novel coronavirus pneumonia (COVID-19) implicate special control measures. J Med Virol 2020;92:568-76.

35. Al-Olama M, Rashid A, Garozzo D. COVID-19-associated meningoencephalitis complicated with intracranial hemorrhage: a case report. Acta Neurochir (Wien) 2020;162:1495-9.

36. Romero-Sánchez CM, Díaz-Maroto I, Fernández-Díaz E, et al. Neurologic manifestations in hospitalized patients with COVID-19: The ALBACOVID registry. Neurology 2020;95:e1060-70.

37. Dalakas MC. Guillain-Barré syndrome: The first documented COVID-19-triggered autoimmune neurologic disease: More to come with myositis in the offing. Neurol Neuroimmunol Neuroinflamm 2020:7.

38. Shridharani AN, Brant WO. The treatment of erectile dysfunction in patients with neurogenic disease. Transl Androl Urol 2016;5:88-101.

39. Sivritepe R, Uçak Basat S, Baygul A, Küçük EV. The effect of interleukin-6 level at the time of hospitalisation on erectile functions in hospitalised patients with COVID-19. Andrologia 2022;54:e14285.

40. Saad HM, GamalEl Din SF, Elbokl OM, Adel A. Predictive factors of erectile dysfunction in Egyptian individuals after contracting COVID-19: a prospective case-control study. Andrologia 2022;54:e14308.

41. Harirugsakul K, Wainipitapong S, Phannajit J, Paitoonpong L, Tantiwongse K. Erectile dysfunction after COVID-19 recovery: a follow-up study. PLoS One 2022;17:e0276429.

42. Costantini E, Trama F, Villari D, et al. The impact of lockdown on couples' sex lives. J Clin Med 2021;10:1414.

43. Fang D, Peng J, Liao S, et al. An online questionnaire survey on the sexual life and sexual function of chinese adult men during the coronavirus disease 2019 epidemic. Sex Med 2021;9:100293.

44. Omar SS, Dawood W, Eid N, Eldeeb D, Munir A, Arafat W. Psychological and sexual health during the covid-19 pandemic in egypt: are women suffering more? Sex Med 2021;9:100295.

45. Değer MD, Madendere S. Erectile dysfunction treatment with Phosphodiesterase-5 Inhibitors: Google trends analysis of last 10 years and COVID-19 pandemic. Arch Ital Urol Androl 2021;93:361-5.

46. Hernandez I, Gul Z, Gellad WF, Davies BJ. Marked increase in sales of erectile dysfunction medication during COVID-19. J Gen Intern Med 2021;36:2912-4.

47. Duran MB, Yildirim O, Kizilkan Y, et al. Variations in the number of patients presenting with andrological problems during the coronavirus disease 2019 pandemic and the possible reasons for these variations: a multicenter study. Sex Med 2021;9:100292.

48. Bulut EC, Ertaş K, Bulut D, Koparal MY, Çetin S. The effect of COVID-19 epidemic on the sexual function of healthcare professionals. Andrologia 2021;53:e13971.

49. Mazza MG, De Lorenzo R, Conte C, et al. COVID-19 biob outpatient clinic study group. anxiety and depression in COVID-19 survivors: role of inflammatory and clinical predictors. Brain Behav Immun 2020;89:594-600.

50. Taquet M, Luciano S, Geddes JR, Harrison PJ. Bidirectional associations between COVID-19 and psychiatric disorder: retrospective cohort studies of 62 354 COVID-19 cases in the USA. Lancet Psychiatry 2021;8:130-40.

51. Nobre P, Rosa PJ, Vasconcelos P, et al. Sexual health and the pandemic crisis: testing the role of psychological vulnerability/protective factors on sexual functioning and sexual distress during a critical life period in portugal. Arch Sex Behav 2022;51:169-81.

52. Pennanen-Iire C, Prereira-Lourenço M, Padoa A, et al. Sexual health implications of covid-19 pandemic. Sex Med Rev 2021;9:3-14.

53. Culha MG, Demir O, Sahin O, Altunrende F. Sexual attitudes of healthcare professionals during the COVID-19 outbreak. Int J Impot Res 2021;33:102-9.

54. Lau WK, Ngan LH, Chan RC, Wu WK, Lau BW. Impact of COVID-19 on pornography use: evidence from big data analyses. PLoS One 2021;16:e0260386.

55. Masoudi M, Maasoumi R, Bragazzi NL. Effects of the COVID-19 pandemic on sexual functioning and activity: a systematic review and meta-analysis. BMC Public Health 2022;22:189.

56. Andersson KE. Mechanisms of penile erection and basis for pharmacological treatment of erectile dysfunction. Pharmacol Rev 2011;63:811-59.

57. Doobay MF, Talman LS, Obr TD, Tian X, Davisson RL, Lazartigues E. Differential expression of neuronal ACE2 in transgenic mice with overexpression of the brain renin-angiotensin system. Am J Physiol Regul Integr Comp Physiol 2007;292:R373-81.

58. Harmer D, Gilbert M, Borman R, Clark KL. Quantitative mRNA expression profiling of ACE 2, a novel homologue of angiotensin converting enzyme. Febs Lett 2002;532:107-10.

59. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol 2002;39:1890-900.

60. Tai AP, Leung MK, Lau BW, Ngai SP, Lau WK. Olfactory dysfunction: a plausible source of COVID-19-induced neuropsychiatric symptoms. Front Neurosci 2023;17:1156914.

61. Giuliano F, Rampin O. Neural control of erection. Physiol Behav 2004;83:189-201.

62. Dominguez JM, Hull EM. Dopamine, the medial preoptic area, and male sexual behavior. Physiol Behav 2005;86:356-68.

63. Pfaus JG. Pathways of sexual desire. J Sex Med 2009;6:1506-33.

64. Arendash GW, Gorski RA. Effects of discrete lesions of the sexually dimorphic nucleus of the preoptic area or other medial preoptic regions on the sexual behavior of male rats. Brain Res Bull 1983;10:147-54.

65. Giuliano F, Rampin O, Brown K, Courtois F, Benoit G, Jardin A. Stimulation of the medial preoptic area of the hypothalamus in the rat elicits increases in intracavernous pressure. Neurosci Lett 1996;209:1-4.

66. Giuliano F, Rampin O. Central neural regulation of penile erection. Neurosci Biobehav Rev 2000;24:517-33.

67. Ziuzia-Januszewska L, Januszewski M. Pathogenesis of olfactory disorders in COVID-19. Brain Sci 2022;12:449.

68. Argiolas A, Melis MR. Neuromodulation of penile erection: an overview of the role of neurotransmitters and neuropeptides. Prog neurobiol 1995;47:235-55.

69. Liu Y, Salamone JD, Sachs BD. Impaired sexual response after lesions of the paraventricular nucleus of the hypothalamus in male rats. Behav Neurosci 1997;111:1361-7.

70. Hernández VS, Zetter MA, Guerra EC, et al. ACE2 expression in rat brain: Implications for COVID-19 associated neurological manifestations. Exp Neurol 2021;345:113837.

71. Mackay A. A paradigm for Post-Covid-19 fatigue syndrome analogous to ME/CFS. Front Neurol 2021;12:701419.

72. Rosenzweig I, Mitrečić D, Petanjek Z, et al. Does damage to hypothalamic paraventricular nucleus underlie symptoms of ultradian rhythm disorder and an increased anxiety in coronavirus disease 2019? Croat Med J 2020;61:377-80.

73. Ward LM. The thalamus: gateway to the mind. Wiley Interdiscip Rev Cogn Sci 2013;4:609-22.

74. Calabrò RS, Cacciola A, Bruschetta D, et al. Neuroanatomy and function of human sexual behavior: a neglected or unknown issue? Brain Behav 2019;9:e01389.[PMID:31706919 DOI: 10.1002/brb3.1389] Caution!.

75. Temel Y, van Lankveld JJ, Boon P, Spincemaille GH, van der Linden C, Visser-Vandewalle V. Deep brain stimulation of the thalamus can influence penile erection. Int J Impot Res 2004;16:91-4.

76. Chen R, Wang K, Yu J, et al. The spatial and cell-type distribution of SARS-CoV-2 receptor ACE2 in the human and mouse brains. Front Neurol 2020;11:573095.

77. Lanuza E, Novejarque A, Martínez-Ricós J, Martínez-Hernández J, Agustín-Pavón C, Martínez-García F. Sexual pheromones and the evolution of the reward system of the brain: the chemosensory function of the amygdala. Brain Res Bull 2008;75:460-6.

78. Baird AD, Wilson SJ, Bladin PF, Saling MM, Reutens DC. Neurological control of human sexual behaviour: insights from lesion studies. J Neurol Neurosur Ps 2007;78:1042-9.

79. Sansone A, Mollaioli D, Limoncin E, et al. The Sexual Long COVID (SLC): erectile dysfunction as a biomarker of systemic complications for COVID-19 long haulers. Sex Med Rev 2022;10:271-85.

80. Ellul MA, Benjamin L, Singh B, et al. Neurological associations of COVID-19. Lancet Neurol 2020;19:767-83.

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OAE Style

Lau BM, Lee JD, Sanchez-Vidaña DI, Chan JM, Lau WW, So KF. The Neural correlates of COVID-19-induced erectile dysfunction in males. Ageing Neur Dis 2023;3:8.

AMA Style

Lau BM, Lee JD, Sanchez-Vidaña DI, Chan JM, Lau WW, So KF. The Neural correlates of COVID-19-induced erectile dysfunction in males. Ageing and Neurodegenerative Diseases. 2023; 3(2): 8.

Chicago/Turabian Style

Benson Wui-Man Lau, Jada Chia-Di Lee, Dalinda-Isabel Sanchez-Vidaña, Jackie Ngai-Man Chan, Way Kwok-Wai Lau, Kwok-Fai So. 2023. "The Neural correlates of COVID-19-induced erectile dysfunction in males" Ageing and Neurodegenerative Diseases. 3, no.2: 8.

ACS Style

Lau, B.M.; Lee J.D.; Sanchez-Vidaña D.I.; Chan J.M.; Lau W.W.; So K.F. The Neural correlates of COVID-19-induced erectile dysfunction in males. Ageing. Neur. Dis. 2023, 3, 8.

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