Cold sores and genital herpes often sit on opposite ends of public perception. One is seen as a minor nuisance, the other as a deeply stigmatized condition. Yet both are caused by nearly identical viruses that affect billions of people worldwide. Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are common, lifelong infections that often go unnoticed due to mild or absent symptoms, but they’re far from rare or shameful.
Much of the confusion begins with how we talk about these viruses. HSV-1 has long been linked to cold sores around the mouth, while HSV-2 is typically associated with genital sores. However, in reality, either virus can appear in either location. Oral-genital contact has led to a rise in genital herpes cases caused by HSV-1, and though less frequent, HSV-2 can also cause oral infections. In some studies, nearly a third of individuals living with herpes were found to carry both types, further blurring the lines between what many assume are separate conditions.
This post unpacks the difference between cold sores and genital herpes by looking beyond surface-level assumptions. We’ll explore how HSV-1 and HSV-2 actually behave, what sets them apart, how each is transmitted, and why the stigma around genital herpes continues to persist despite the viruses being so alike. With greater clarity comes the opportunity for better understanding, less fear, and more compassionate conversations.
Understanding the Herpes Simplex Virus: HSV-1 vs. HSV-2
Herpes simplex virus exists in two forms: HSV-1 and HSV-2. Although genetically distinct, these viruses are closely related and capable of causing infections in both oral and genital regions. Their names reflect historical patterns more than current behavior.
HSV-1 has traditionally been linked to cold sores around the mouth, commonly acquired in childhood. However, it has become an increasingly common cause of genital herpes, particularly in high-income countries. Changes in sexual behavior, including more frequent oral-genital contact, have led to a sharp rise in genital HSV-1 infections, especially among young people who were not previously exposed to the virus as children.
HSV-2, on the other hand, remains the primary cause of genital herpes. It rarely appears in the oral region, even in people who engage in oral-genital sex. While oral HSV-2 infections are possible, they are quite uncommon. This difference in location preference is one of the few consistent distinctions between the two viruses.
Still, it’s important to stress that the location of infection does not determine the virus type. Either HSV-1 or HSV-2 can infect either area. Cases of HSV-1 spreading from the mouth to the genitals without any sexual contact, such as by touching a sore and then another part of the body, illustrate this clearly.
Both types of herpes share transmission pathways and the ability to lie dormant in nerve cells, reactivating occasionally. The real differences lie in how often they recur and where they tend to reactivate. HSV-2 more frequently causes recurring genital outbreaks, while HSV-1 is often less persistent, especially when it infects the genital area.
This overlap in behavior, combined with shifting transmission trends, makes it essential to move away from outdated assumptions. Understanding that either virus can cause similar symptoms in different places helps reduce stigma and encourages more accurate, compassionate conversations.
Symptoms: What’s Similar and What’s Unique
Whether caused by HSV-1 or HSV-2, herpes infections often begin with a recognizable pattern. The first outbreak is typically the most intense, marked by tingling, itching, or burning at the site of infection. These sensations are followed by small fluid-filled blisters that can rupture and turn into painful sores. Many people also experience flu-like symptoms such as fever, swollen lymph nodes, headaches, muscle aches, and general fatigue, especially during an initial episode.
This early phase is similar across both types and infection sites. People with oral herpes often report a tingling or burning sensation before cold sores appear, highlighting the shared prodrome of HSV infections. These symptoms signal that the virus is active and traveling along the nerves toward the skin’s surface.
Oral herpes, most often caused by HSV-1, tends to present as sores on the lips, gums, tongue, or surrounding areas of the face. These outbreaks are frequently triggered by sun exposure, emotional stress, or illness, and are usually mild and self-limiting. In healthy individuals, cold sores typically clear up within two to three weeks. For those with weakened immune systems, however, symptoms may be more severe and longer lasting.
Genital herpes can be caused by either HSV-1 or HSV-2, though HSV-2 remains the more common cause. This form appears as painful blisters or ulcers on the genitals, thighs, buttocks, or around the anus. The first outbreak may also involve fever, headache, painful urination, and swollen glands. Notably, only a minority of those infected will have noticeable symptoms, yet even mild or unrecognized episodes can still be contagious.
The intensity and frequency of outbreaks often vary depending on the virus type and location. HSV-2 tends to cause more severe and frequent recurrences, particularly in the genital area. In contrast, genital HSV-1 infections are typically milder and recur less often. Over time, both types tend to flare up less frequently, especially when managed with antiviral medication.
Recognizing these patterns helps individuals better understand their condition and manage it more confidently. Whether on the mouth or the genitals, caused by HSV-1 or HSV-2, the core experiences overlap far more than they differ.
Transmission: How Each Type Spreads
Herpes simplex virus spreads in ways that are often misunderstood, with patterns that differ slightly between HSV-1 and HSV-2.
HSV-1 is most commonly transmitted through nonsexual contact, especially during childhood. This includes everyday interactions like kissing or sharing cups and utensils. In fact, global studies estimate that nearly two-thirds of people under age 50 carry HSV-1, often without knowing it. Many children contract the virus from caregivers during routine, affectionate moments like a kiss on the lips. Because HSV-1 can be passed on even when no symptoms are visible, it often spreads quietly and early in life.
HSV-2, in contrast, is typically acquired later and almost always through sexual contact. It is most commonly spread via vaginal, anal, or oral sex. The risk of contracting HSV-2 increases with the number of sexual partners and a history of other sexually transmitted infections. In population studies, HSV-2 is rarely found in people who are not sexually active, reinforcing its status as a sexually transmitted infection.
Despite these differences, both HSV-1 and HSV-2 can be transmitted through oral-genital contact. Genital HSV-1 infections have become increasingly common, particularly among younger adults, due to changes in sexual practices. Skin-to-skin contact is enough to spread the virus, and this can happen even when there are no visible sores. This is because of a phenomenon known as viral shedding, where the virus is present on the skin surface without causing symptoms.
Asymptomatic shedding is one of the main reasons herpes continues to spread silently. Both HSV-1 and HSV-2 can shed virus particles unpredictably, not just during outbreaks. Shedding is more frequent in the days surrounding an outbreak, but it can also occur without warning. This makes transmission possible even when someone feels completely fine. Antiviral medications can help reduce the frequency of shedding but do not eliminate it entirely.
Understanding how these viruses spread—both visibly and invisibly—helps reduce the stigma often attached to them. It also underscores the importance of honest conversations, regular testing, and informed prevention strategies.
Recurrence Patterns and Triggers
While both HSV-1 and HSV-2 can remain dormant in the body and reactivate periodically, their recurrence patterns differ, particularly when it comes to genital infections.
Genital HSV-1 infections tend to recur much less frequently than those caused by HSV-2. In one study, only a quarter of individuals with genital HSV-1 experienced recurrent outbreaks, compared to nearly 90 percent of those with HSV-2. This trend has been confirmed in animal studies and in research showing that HSV-1 establishes lower levels of latent viral DNA in genital nerve clusters. The result is a lower likelihood of the virus reactivating in the genital area.
HSV-2, by contrast, is known for its higher recurrence rate, especially in genital tissues. It can reactivate as often as several times a year, with recurrences often presenting as lesions similar to the initial outbreak. This more persistent pattern is linked to HSV-2’s stronger ability to replicate and reactivate within both sensory and autonomic nerve clusters. Even in controlled studies with animals, HSV-2 produced more frequent and longer-lasting lesions than HSV-1.
Despite these differences, the triggers that can reactivate the virus are largely the same for both types. Common factors include emotional stress, illness, menstrual cycles, friction, and exposure to sunlight or UV light. These triggers can prompt the virus to travel from its dormant state in the nerve ganglia back to the skin, where it causes visible symptoms. Autonomic nerves, which respond to stress and hormonal changes, play a key role in this process.
Even long after the initial infection, stress remains a powerful and well-documented trigger for reactivation. People may find that outbreaks are more likely to happen during periods of physical or emotional strain, even years after the first episode.
Recognizing these patterns and what influences them can help individuals anticipate and manage outbreaks more effectively. Though HSV-2 tends to be more active in the genital area, both virus types respond to similar physiological cues, making awareness a useful tool for living well with either infection.
Emotional and Social Stigma: Why It’s Worse for Genital Herpes
The contrast in how oral and genital herpes are perceived is striking. Cold sores, most often caused by HSV-1, are generally accepted as a harmless inconvenience. They are rarely viewed through a sexual lens. Genital herpes, usually caused by HSV-2, is treated quite differently. It is often associated with shame, secrecy, and moral judgment, despite being caused by a virus that behaves similarly to its oral counterpart.
Many people do not connect cold sores with herpes, even though both HSV-1 and HSV-2 belong to the same viral family. Because oral herpes is often acquired in childhood through casual contact like kissing, it tends to be seen as innocent or unrelated to sexual behavior. Genital herpes, by contrast, is strongly linked to sexual transmission and often viewed as a reflection of personal choices. This perception leads to deeper stigma and emotional distress.
Medically, there is little that separates the two. HSV-1 and HSV-2 are nearly identical in structure, share similar symptoms, and respond to the same treatments. The differences lie mainly in where the virus prefers to reside and how frequently it reactivates. The stigma surrounding genital herpes is not based on clinical evidence but shaped instead by cultural attitudes, lack of education, and fear.
This stigma can take a heavy toll. People living with genital herpes may struggle with anxiety, depression, or fear of rejection. These feelings are often amplified by the silence that surrounds the condition and by the belief that it somehow defines a person’s worth or character.
Reducing this stigma benefits everyone. When herpes is understood as a common and manageable virus, it opens the door to better communication, safer sex, and healthier relationships. Education that clarifies the reality of both HSV-1 and HSV-2 can help shift the focus from judgment to support, creating space for compassion and connection over fear and shame.
Diagnosis and Testing Considerations
Accurate testing plays a key role in managing herpes simplex virus. It helps confirm a diagnosis, determine the type of virus present, and guide both treatment decisions and conversations about transmission.
Swab-based testing, particularly using PCR (polymerase chain reaction), is considered the most reliable method when active sores are present. PCR testing detects the genetic material of the virus and can distinguish between HSV-1 and HSV-2 with a high degree of accuracy. These tests are not only faster than older methods like viral culture but also far more sensitive, making them the gold standard for identifying herpes in clinical settings.
For people without visible symptoms, blood tests that detect HSV-specific antibodies are commonly used. These type-specific serologic tests rely on glycoprotein G to identify whether a person has been previously exposed to HSV-1 or HSV-2. While they cannot determine the site of infection, they can confirm past exposure even when no symptoms have occurred.
Understanding which type of HSV someone has is medically important. Genital infections caused by HSV-1 usually recur less often than those caused by HSV-2. This distinction matters when counseling patients about what to expect and whether long-term antiviral therapy might be beneficial. For example, suppressive treatment is more commonly recommended for HSV-2 due to its higher rates of recurrence and asymptomatic shedding.
In certain situations, such as during pregnancy, knowing the HSV type can be especially critical. If a pregnant person acquires HSV for the first time near delivery, the risk to the newborn can be much higher—particularly if they have no existing antibodies to either virus. Early detection and accurate typing allow for more informed care and preventative strategies during birth.
Testing is not just about confirming a diagnosis. It supports better decision-making, encourages honest communication, and helps reduce fear by replacing uncertainty with knowledge.
Treatment and Management: Largely the Same
Both HSV-1 and HSV-2 respond well to antiviral medications that target the virus’s ability to replicate. These treatments can ease symptoms, speed healing during outbreaks, and reduce the chances of passing the virus to others.
Oral antiviral medications such as acyclovir, valacyclovir, and famciclovir are commonly prescribed for both types of herpes. They work by inhibiting viral DNA replication and are effective whether the infection is oral or genital. Among these, valacyclovir is often favored for its longer-lasting effects and ability to reduce both recurrence and viral shedding. Regardless of type, treatment success depends in part on how much of the drug reaches the area where the virus reactivates.
For people who experience frequent or severe outbreaks, daily suppressive therapy is available. Taking antivirals consistently can significantly lower the risk of outbreaks and reduce asymptomatic viral shedding. This approach is especially useful for managing HSV-2, which tends to reactivate more frequently than HSV-1. Suppressive treatment can also lower the chances of transmission, although it does not eliminate the risk entirely.
Lifestyle choices also play a meaningful role in managing herpes. Psychological stress, lack of sleep, and poor immune function are known triggers for reactivation. Managing stress and getting adequate rest can help keep the virus in check. While no specific diet can cure or prevent herpes, maintaining a balanced, nutrient-rich diet and avoiding personal triggers may help reduce the frequency of flare-ups.
Effective herpes management is about more than just medication. A combination of antiviral therapy and supportive lifestyle habits offers the best results, helping individuals maintain control over their symptoms while reducing the risk of passing the virus to others.
Can Oral Herpes Become Genital (or Vice Versa)?
Yes, although it is uncommon, oral herpes can become genital and vice versa through a process called autoinoculation. This refers to the self-transfer of the herpes virus from one part of the body to another. It is most likely to happen during a person’s first outbreak, when the immune system has not yet built antibodies and viral load is at its highest. People who are unaware they have herpes may accidentally spread the virus by touching a sore and then another mucosal area, such as the eyes or genitals. Though rare, this can lead to complications like herpetic eye infections or herpetic whitlow on the fingers.
Far more often, transmission occurs between partners, especially through oral sex. HSV-1, traditionally associated with cold sores, is now a leading cause of genital herpes among young adults. Many new cases are linked to oral-genital contact, particularly among individuals who consider oral sex to be lower risk and choose not to use protection. This shift reflects changing sexual behaviors and highlights the importance of including HSV-1 in discussions about sexual health.
To lower the risk of transmission, using condoms and dental dams is strongly recommended. While not foolproof, these barriers help reduce direct skin-to-skin contact, which is how herpes spreads. Studies suggest that condom use can cut the risk of HSV transmission by about 30 to 50 percent. Adding daily antiviral therapy to barrier protection further decreases the likelihood of passing the virus to a partner.
Understanding that herpes can move between different parts of the body and between partners in various ways helps people make more informed choices. With the right precautions, the risk of transmission can be significantly reduced.
Bringing Clarity to a Common Confusion
Herpes can be a tricky topic, not because the science is unclear, but because the conversation around it so often is. This article has walked through the core facts: HSV-1 and HSV-2 are closely related viruses that can affect either the mouth or the genitals. While they differ in how often they recur or where they prefer to live, both are manageable, common, and far less scary than stigma makes them seem.
The truth is, many people live with herpes, often without knowing it, and lead full, healthy lives. By separating fact from fear and recognizing that neither type defines a person’s worth or identity, we create more space for compassion, honesty, and better health choices.
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References
A, D., M.D, A.R., G, J.F., Rehan, A.D., R.S, P., & J, V. (2020). ANALYSIS OF HERPES SIMPLEX VIRUS USING GINGIVAL CREVICULAR FLUID- A REVIEW. Journal of Indian Dental Association Madras.
Aymard M. (2002). Epidémiologie actuelle de l’herpès [Current epidemiology of herpes]. Pathologie-biologie, 50(7), 425–435.
Barnack-Tavlaris, J. L., Reddy, D. M., & Ports, K. (2011). Psychological adjustment among women living with genital herpes. Journal of health psychology, 16(1), 12–21.
Bartlett, J. (2004). Recent developments in the management of herpes simplex virus infection in HIV-infected persons. Clinical Infectious Diseases, 39(Suppl 5), S237-S239.
Bellizzi, A., Fioriti, D., Marcone, V., Anzivino, E., Mischitelli, M., Barucca, V., Parisi, A., Moreira, E., Osborn, J., Chiarini, F., Calzolari, E., & Pietropaolo, V. (2009). Epidemiology of Herpes Simplex Virus Infection in Pregnancy: A Pilot Study. European Journal of Inflammation, 7, 161–168.
Bernstein, D., Stanberry, L., Harrison, C., Kappes, J., & Myers, M. (1986). Antibody response, recurrence patterns and subsequent herpes simplex virus type 2 (HSV-2) re-infection following initial HSV-2 infection. The Journal of General Virology, 67(Pt 8), 1601–1612.
Brown, Z. A., Selke, S., Zeh, J., Kopelman, J., Maslow, A., Ashley, R. L., & Corey, L. (2003). The acquisition of HSV during pregnancy. New England Journal of Medicine, 337(8), 509–515.
Centers for Disease Control and Prevention. (2023). Genital Herpes – CDC Fact Sheet (Detailed).
Chayavichitsilp, P., Buckwalter, J. V., Krakowski, A. C., & Friedlander, S. F. (2009). Herpes simplex. Pediatrics in Review, 30(4), 119–129.
Docherty, J. J., Trimble, J. J., Roman, S., Faulkner, S. C., Naugle, F. P., Mundon, F. K., & Zimmerman, D. H. (1985). Lack of oral HSV-2 in a college student population. Journal of Medical Virology, 16.
Engel, J. (2017). Suppressive antiviral medication should be counseled that they may still transmit HSV to their sexual partners.
Farooq, A. V., & Shukla, D. (2012). Herpes simplex epithelial and stromal keratitis: An epidemiologic update. Survey of Ophthalmology, 57(5), 448–462.
Groves, M. J. (2016). Genital herpes: A review. American Family Physician, 93(11), 928-934.
Herpes Genital. (2012). HERPES GENITAL. Una actualización para el profesional.
James, C., Harfouche, M., Welton, N. J., Turner, K. M., Abu-Raddad, L. J., & Looker, K. J. (2020). Herpes simplex virus: Global infection prevalence and incidence estimates, 2016. Bulletin of the World Health Organization, 98(5), 315-329.
Johnston, C., & Corey, L. (2016). Current Concepts for Genital Herpes Simplex Virus Infection: Diagnostics and Pathogenesis of Genital Tract Shedding. Clinical microbiology reviews, 29(1), 149–161.
Johnston, C.M., Magaret, A.S., Son, H., Stern, M.E., Rathbun, M.M., Renner, D.W., Szpara, M.L., Gunby, S.A., Ott, M., Jing, L., Campbell, V.L., Huang, M.W., Selke, S.S., Jerome, K.R., Koelle, D.M., & Wald, A. (2022). Viral Shedding 1 Year Following First-Episode Genital HSV-1 Infection. JAMA.
Kimberlin, D. W., & Whitley, R. J. ( 2007). Antiviral therapy of HSV-1 and -2. In A. Arvin (Eds.) et. al., Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press.
Kimberlin D. W. (2004). Neonatal herpes simplex infection. Clinical microbiology reviews, 17(1), 1–13.
Lafferty, W., Coombs, R., Benedetti, J., Critchlow, C., & Corey, L. (1987). Recurrences after oral and genital herpes simplex virus infection: Influence of site of infection and viral type. The New England Journal of Medicine, 316(23), 1444-1449.
Le Cleach, L., Trinquart, L., Do, G., Maruani, A., Lebrun-Vignes, B., Ravaud, P., & Chosidow, O. (2014). Oral antiviral therapy for prevention of genital herpes outbreaks. The Cochrane Database of Systematic Reviews, 8, CD009036.
Lee, A. S. D., & Cody, S. L. (2020). The Stigma of Sexually Transmitted Infections. The Nursing clinics of North America, 55(3), 295–305.
Lee, S., Ives, A. M., & Bertke, A. S. (2015). Herpes Simplex Virus 1 Reactivates from Autonomic Ciliary Ganglia Independently from Sensory Trigeminal Ganglia To Cause Recurrent Ocular Disease. Journal of virology, 89(16), 8383–8391.
Lekstrom-Himes, J. A., Pesnicak, L., & Straus, S. E. (1998). The quantity of latent viral DNA correlates with the relative rates at which herpes simplex virus types 1 and 2 cause recurrent genital herpes outbreaks. Journal of virology, 72(4), 2760–2764.
Liu, J., Yi, Y., Chen, W., Si, S., Yin, M., Jin, H., Liu, J., Zhou, J., & Zhang, J. (2015). Development and evaluation of the quantitative real-time PCR assay in detection and typing of herpes simplex virus. International Journal of Clinical and Experimental Medicine, 8(10), 18758–18764.
Looker, K. J., Magaret, A. S., Turner, K. M., Vickerman, P., Gottlieb, S. L., & Newman, L. M. (2015). Global estimates of prevalent and incident herpes simplex virus type 1 infections in 2012. PLoS One, 10(5), e0129883.
Malkin, J. (2002). Natural history of HSV1 and HSV2 transmission and implications for HIV. Annales de Dermatologie et de Venereologie, 129(4 Pt 2), 571-576.
Manzano, G. S., Danish, H. H., Chu, C. J., & Kimchi, E. Y. (2021). Child Neurology: Intractable Epilepsy and Transient Deficits in a Patient With a History of Herpes Simplex Virus Encephalitis. Neurology, 96(14), 679–681.
Martin, E. T., Krantz, E., Gottlieb, S. L., Magaret, A. S., Langenberg, A., Stanberry, L., Kamb, M., & Wald, A. (2009). A pooled analysis of the effect of condoms in preventing HSV-2 acquisition. Archives of internal medicine, 169(13), 1233–1240.
Patel, R., Stanberry, L., & Whitley, R. (2007). Review of recent HSV recurrent-infection treatment studies. Herpes: the journal of the IHMF, 14(1), 23-26.
Paz-Bailey, G., Ramaswamy, M., Hawkes, S., & Geretti, A. (2007). Herpes simplex virus type 2: epidemiology and management options in developing countries. Sexually Transmitted Infections, 83(1), 16–22.
Pereira, D., & Sannes, T. (2020). Genital Herpes. Encyclopedia of Behavioral Medicine.
Pero, M., & Espinós, J. J. (2016). Genital Herpes Simplex Virus Type 1: Case report of oro-genital infection by autotransmission.
Raborn, G. W., & Grace, M. G. (2003). Recurrent herpes simplex labialis: selected therapeutic options. Journal (Canadian Dental Association), 69(8), 498–503.
Ramalho, K. M., Cunha, S., Gonçalves, F., Silva Escudeiro, G., Steiner-Oliveria, C., Horliana, A., & Eduardo, C. (2020). Photodynamic therapy and Acyclovir in the treatment of recurrent herpes labialis. Photodiagnosis and Photodynamic Therapy, 102093.
Rapp, F. (1981). Herpes Simplex Virus Infections. Part 1. How Widespread They Are, and Who H Most Threatened.
Rozenberg, F., Deback, C., & Agut, H. (2011). Herpes simplex encephalitis : from virus to therapy. Infectious disorders drug targets, 11(3), 235–250.
Sauerbrei, A. (2018). Genital Herpes. Diagnostics to Pathogenomics of Sexually Transmitted Infections.
Setyowati, D., Prihanti, A. M., & Adi, A. M. S. (2023). Diagnosis and Treatment of Recurrent Herpes Labialis. International Journal of Medical Science and Clinical Research Studies.
Silva, A.M. (2015). Perfil epidemiológico do Herpes simplex no grupo de homens que fazem sexo com homens e avaliação do RNA de interferência como agente antiviral na encefalite herpética em camundongos BALB/c.
Skelly, M. J., Burger, A., & Adekola, O. (2012). Herpes Simplex Virus-1 Encephalitis: A Review of Current Disease Management. Antiviral Chemistry and Chemotherapy, 23, 13–18.
Slinger, R., Amrud, K., Sant, N., Ramotar, K., & Desjardins, M. (2019). A comparison of molecular methods for HSV-1 and HSV-2 detection from swab specimens. Journal of Clinical Virology, 113, 35–38.
Stanberry, L., Kern, E., Richards, J., & Overall, J. (1985). Recurrent genital herpes simplex virus infection in guinea pigs. Intervirology, 24(4), 226–231.
Tobian, A. A., & Quinn, T. C. (2009). Herpes simplex virus type 2 and syphilis infections with HIV: an evolving synergy in transmission and prevention. Current opinion in HIV and AIDS, 4(4), 294–299.
Tronstein, E., Johnston, C., Huang, M.-L., Selke, S., Magaret, A., Warren, T., Corey, L., & Wald, A. (2011). Genital shedding of herpes simplex virus among symptomatic and asymptomatic persons with HSV-2 infection. JAMA, 305(14), 1441–1449.
Wald, A. (2006). Genital HSV-1 infections. Sexually Transmitted Infections, 82, 189–190.
Wald, A., & Link, K. (2002). Risk of human immunodeficiency virus infection in herpes simplex virus type 2–seropositive persons: A meta-analysis. Journal of Infectious Diseases, 185(1), 45–52.
Wilson, M., & Wilson, P. J. K. (2021). Cold Sores. Close Encounters of the Microbial Kind.
Workowski, K. A., & Bachmann, L. H. (2021). Sexually transmitted infections treatment guidelines, 2021. MMWR Recommendations and Reports, 70(4), 1–187.
World Health Organization. (2022). Herpes simplex virus.
Xu, F., Sternberg, M. R., Kottiri, B. J., McQuillan, G. M., Lee, F. K., Nahmias, A. J., Berman, S. M., & Markowitz, L. E. (2006). Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA, 296(8), 964–973.
Young, H., & Ogilvie, M. (1994). Herpes simplex virus (HSV-1; HSV-2) (Genital herpes). In Sexually Transmitted Infections (pp. 184–238).
Zuckerman, R., Lucchetti, A., Whittington, W., et al. (2009). HSV suppression reduces seminal HIV-1 levels in co-infected men. AIDS, 23, 479-483.