Well, that was an awkward moment. I had never thought that it would actually happen. From childhood, I as an innocent boy always considered a kiss as the most sensual thing the human body could do. The romantic lingering of the eyes sets the scene, with classical jazz playing in the background. Wrapping each other's arms around the corpo, savouring the carnal warmth that arises from the depth of one's most profound desires. She is my crush but we have stayed friends for quite a while (for those offering their condolences, I've been listening to 'Obvious' by Westlife for the fifteen millionth time). Our lips touched for the first time. I thought it would be a messy moment for both of us, but it turned out to be quite smooth. Our tongues touched. A few seconds later, she started biting my lower lip and I licked her lips with my tongue, pulling her closer to my chest. Our noses touched and she kissed my eyes. I did the same. We explored each other's faces for quite some time before the striking of the grandfather clock announced the arrival of the sixth hour. Realising that my time was up, I packed my things and gave her a gentle kiss on the cheek before bidding farewell. I would never forget the lingering smile on her face. A few weeks later, I was restrained in bed in a giant onesie, wrapped in a blanket with a mug of hot chocolate. I also discovered a firm lump on my neck. I never called her again.
Anyway, what happened? These symptoms did not happen all at once. Rather, they assumed a gradual, temporal occurrence. First, I noticed I was extremely tired all the time. It was different from the ordinary bumblebee type of malaise which happens to all medics who are tirelessly running up and down the hospital, traversing between wards ruled by almighty consultants. It was a general feeling of discomfort, that prompted me to confine myself to the premises of my bedroom day after day. I am not joking when I nearly hit a patient's head with my falling tendon hammer when I was checking for his pulse. I was so exhausted that even a passing doctor asked me if I was alright. At the time, I thought it was a minor issue - something resolvable with twelve hours of sleep. I was wrong. It got worse. To the extent that I was unable to concentrate. My psychiatry tutor stared at me in utter disbelief when I said a psychotic patient should be given amphetamine at the peak of my exhaustion (amphetamine is a stimulant and what a psychotic patient needs is a tranquiliser). I then developed a low-grade fever (in medicine, there are low-grade and high-grade fevers, each indicative of different pathologies, but not necessarily; usually, high fevers indicate an acute infection, possibly culminating, but not essentially, sepsis; low-grade fevers point more towards chronic infections and inflammatory processes, including cancers and tuberculosis). I always felt hot all over and sweated profusely when covering myself with a fleece blanket during the night. Living alone, I started to panic what would happen to me. Would it be COVID-19? I panicked. However, I had no other coryzal symptoms (symptoms associated with inflammation of the mucosal membranes of the nasal cavity, including runny nose, sneezing and coughing) which are usually found in patients with COVID-19. At the same time, I developed a sore throat as I finally decided to apply for leave. Trapped in the confines of my small London flat overlooking the doom and gloom of the second lockdown, I treated myself to two movies and consoled myself that it was just common cold. Then, it happened.
I looked into the mirror one day and saw a lump over my neck. It was rather odd and I didn't notice it before. Situated over the anterolateral aspect of my upper neck, just under the jaw, lied a defiant, oval-shaped mass that did not seem to fear the anger of betrayal in my eyes. I observed it more closely. No overlying skin changes. Clear, well-defined contours; singular mass with no associated masses neither on the same side nor the other side of the neck; roughly 2 cm x 1.5 cm in size; not painful (or non-tender, to cite a more medically sophisticated way of delivery), firm in consistency and not pulsatile, nor fluctuant (these two parameters, as mentioned in my previous posts, aren't really useful; however, when dealing with neck masses, a pulsatile one on the side of the neck can be indicative of a rare tumour called carotid body tumour which is associated with the carotid artery, a main neck artery supplying blood to the brain and the wider head and neck region; moreover, 'fluctuant' is usually indicative of fluid-filled cysts - again, there's a rare pathology called branchial cyst which is more common in infants. Both pathologies tend to assume chronicity). Most importantly, it is not tethered to the underlying tissue. This is likely to be an enlarged lymph node. This constellation of symptoms can only mean one important diagnosis - Infectious Mononucleosis.
Lymph Node Groups in the Head and Neck (source: Springer Link).
Some of you might have heard of this disease. In university and college circles, there are several diseases that freshers have to take heed. Infectious mononucleosis is one of them. The others can include meningitis (caused by Neisseria meningitidis, which can be spread by saliva and respiratory droplets, with sporadic cases of sexual transmission [1]), sexually-transmitted infections (think about gonococcal disease and Chlamydia as the chief ones; HIV and Syphilis are the significant yet relatively rare entities) and mumps (which can cause parotid tumours, inflammation of the parotid gland [2] and encephalitis- whole brain inflammation [3]). Infectious mononucleosis, also known as glandular fever, is caused by a virus called Epstein-Barr Virus (EBV) [4]. Viruses are special in their own way - the cool thing about them is that scientists, to this day still debate whether they've actually lived. This might sound like a philosophical question, but it has a sound scientific basis. Viruses are considered non-living once they are outside a host. Once they've identified a host, they latch onto it and never let go. Injecting the poor host (i.e. any poor cell in the proximity, which can be a human somatic cell, or a bacterium) with their genetic material (this sounds like rape if you ask me), such viruses utilise the resources within the cell to reproduce. The genetic material can exist on its own, or combines with that of the host cell, for the purposes of replication. This ensures the perpetuation of their bloodline (although, technically, they don't actually have a 'blood'-line). In this case, viruses have a wide array of methods to make sure they live as long as they could in the host. They can reproduce straight away, reproducing in vast numbers, thus essentially converting the host cell into a virus machine. Or, more intelligently, they can recognise dangers and choose to replicate later. The genetic material of the virus remains separate from that of the cell. This is called an episome. At some chosen point, at the right time, they strike and initiate their proceedings of mass invasion. This is an extremely good strategy since nobody would ever know that they're tucked away in this corner of paradise. Once they don't produce proteins, there is no way for the T Killer Cells and NK Cells (part of the human immune system) to know. These cells contrive to kill host cells but if the viruses go silent, their detection methods, being inherently flawed, deceive them. [5-7]
Viral Reproduction Cycle within Host Cell (extracted from: https://media.istockphoto.com/vectors/virus-replication-cycle-vector-id664748584)
It is true that EBV can replicate rapidly and hide away, happily tucked away in silence until it wants to strike. Extremely common in the general population, EBV can cause a range of illnesses, including a variety of cancers (such as nasopharyngeal carcinomas prevalent in China, Burkitt's Lymphoma, Hodgkin's Lymphoma, and Post-transplant Lymphoproliferative Disorder). It was found that EBV antibodies were present in 85.3% of the general population. The figure is more striking for those in the 20-25 years age-bracket, amping up to 96.0%. [8-9] It transpires that the main route of EBV transmission is kissing, thus it's nickname 'kissing disease'. Some might question how kissing has anything got to do with viral transmission. It is a mood-killer for certain to check with your partner whether she/he has EBV before kissing (and indeed many EBV infections are asymptomatic and silent, meaning that they wouldn't have known anyway), but the activity leads to the swapping of saliva. Saliva contains the virus. The effect is augmented in deep kissing. Of course, kissing is not the only way of transmission. There is evidence which suggests that the virus can also be transmitted through blood transfusion, organ transplant and sexual activity (um, I mean, full-blown sexual intercourse involving penetration). [10-11] However, as exhibited in my case, even the deepest type of kissing (I would like to think that tongue-swapping is already pretty extreme) does not immediately confer upon the victim a sick role. It takes roughly 6 weeks for symptoms to arise - we call this period the incubation period. Incubation is the process whereby the virus grows in number. We need to recognise that symptoms only arise when something is not going right. Our definition of going wrong deviates massively from that of the body. Our body only tells us that something is going wrong when there is an actual spanner in the works - rather pragmatic in this respect, not when there is only a cheeky EBV scurrying in the premises. [12] These symptoms arise when EBV enters the tonsils and attacks multiple tissues and cells, including our faithful B Cells (part of the human immune system), liver and spleen. T Killer Cells and NK Cells roar in fury and launch their strong defensives. Such proliferation of immune cells is accompanied by the enlargement of lymph nodes. Finally, EBV admits defeat and seeks refuge from resting B Cells, morphing themselves into episomes until the right moment comes for them to strike again. [13-14]
I have been swamped by messages of encouragement. That's nice, considering that I'm actually nobody special. To be seen as the centre of attention for even a limited period of time feels nice. However, I've also been assaulted by various strands of 'medical advice'. Many suggest that I should go and get some antibiotics, going as far as suggesting that I can sneak into the hospital and get some. Well, for starters, that's stealing. Secondly, many seem to labour under the delusion that viruses can be somehow 'cured' or 'defeated' by antibiotics. These comments come from a very well-meaning place, but at the same time, signs of health misinformation in society are showing. We need to act now to make sure that the health information disseminated on the internet is correct and clear. Antibiotics are only for organisms that are, strictly speaking, living. This applies to bacteria and fungi, for instance. For viruses, whose status as a living thing is still debated, antibiotics do nothing but encourage microbial resistance. This only increases the likelihood of a bacterial-on-viral infection (it is totally possible for the body to be under siege by co-infections- a famous example would be the most ambitious crossover in medical history- HIV and Tuberculosis).
Antibiotics in a Cup - to this day, we're still facing the grave issue of over-medicalisation.
For the majority of viral infections, including COVID-19 (mild disease) [15], there is simply no cure, because it's not required. Drugs such as ritonavir (Hepatitis C), nevirapine (HIV) and entecavir (Hepatitis B) are only used for viral infections which entail serious corporal consequences, that the viral load (amount of virus in the body) is recommended to be lowered to a vanishing extent so that the disease is kept at bay. For minor infections such as influenza and infectious mononucleosis, introducing anti-viral drugs only makes matters worse since these drugs entail serious side effects. Supportive therapy is the only recommended regimen for those with infectious mononucleosis, with regard to the fact that most patients contract the disease when they're in their twenties. Supportive therapy means making one comfortable - take paracetamol for feverish symptoms, drink more water and do regular exercises. Of course, if there is any worsening of symptoms, including the enlargement of the neck mass which possibly obstructs the airway (thus rendering it very difficult to breathe), one would need to go to the hospital to have it sorted. Otherwise, the disease is self-limiting and symptoms disappear within 1-2 weeks. [16]
For those of you who wish me well, my strength is growing and I've once again indulged myself in heaps of chocolate (I seem to get addicted somehow - must be the stupid endorphin and the dopamine surge). However, this has taught me a very important lesson: always choose the right person to kiss.
[1] Ladhani S, Lucidarme J, Parikh S, Campbell H, Borrow R, & Ramsay M. (2020). Meningococcal disease and sexual transmission: urogenital and anorectal infections and invasive disease due to Neisseria meningitidis. The Lancet, 395(10240), 1865-1877. https://doi.org/10.1016/s0140-6736(20)30913-2.
[2] Wilson KF, Meier JD, Ward PD. (2014). Salivary Gland Disorders. Am Fam Physician. 1;89(11):882-888.
[3] Johnstone J, Ross C, & Dunn M. (1972). Meningitis and Encephalitis Associated with Mumps Infection: A 10-Year Survey. Archives Of Disease In Childhood, 47(254), 647-651. https://doi.org/10.1136/adc.47.254.647.
[4] Smatti M, Al-Sadeq D, Ali N, Pintus G, Abou-Saleh H, & Nasrallah G. (2018). Epstein–Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update. Frontiers In Oncology, 8. https://doi.org/10.3389/fonc.2018.00211.
[5] De Leo A, Calderon A, Lieberman PM. (2020). Control of Viral Latency by Episome Maintenance Proteins. Trends in Microbiology, 28(2), 150-162. doi: https://doi.org/10.1016/j.tim.2019.09.002.
[6] Pistello M, & Antonelli G. (2016). Integration of the viral genome into the host cell genome: a double-edged sword. Clinical Microbiology And Infection, 22(4), 296-298. https://doi.org/10.1016/j.cmi.2016.01.022.
[7] Krzewski K, & Coligan J. (2012). Human NK cell lytic granules and regulation of their exocytosis. Frontiers In Immunology, 3. https://doi.org/10.3389/fimmu.2012.00335.
[8] Kuri A, Jacobs B, Vickaryous N, et al. (2020). Epidemiology of Epstein-Barr virus infection and infectious mononucleosis in the United Kingdom. BMC Public Health, 20(1). https://doi.org/10.1186/s12889-020-09049-x.
[9] El-Sharkawy A, Al Zaidan L, & Malki A. (2018). Epstein–Barr Virus-Associated Malignancies: Roles of Viral Oncoproteins in Carcinogenesis. Frontiers In Oncology, 8. https://doi.org/10.3389/fonc.2018.00265.
[10] Dunmire S, Hogquist K, & Balfour H. (2015). Infectious Mononucleosis. Current Topics In Microbiology And Immunology, 211-240. https://doi.org/10.1007/978-3-319-22822-8_9.
[11] Crawford D, Swerdlow A, Higgins C, et al. (2002). Sexual History and Epstein‐Barr Virus Infection. The Journal Of Infectious Diseases, 186(6), 731-736. https://doi.org/10.1086/342596.
[12] Dunmire S, Grimm J, Schmeling D, Balfour H, & Hogquist K. (2015). The Incubation Period of Primary Epstein-Barr Virus Infection: Viral Dynamics and Immunologic Events. PLOS Pathogens, 11(12), e1005286. https://doi.org/10.1371/journal.ppat.1005286.
[13] Kalla M, Gobel C, & Hammerschmidt W. (2011). The Lytic Phase of Epstein-Barr Virus Requires a Viral Genome with 5-Methylcytosine Residues in CpG Sites. Journal Of Virology, 86(1), 447-458. https://doi.org/10.1128/jvi.06314-11.
[14] Prang N, Hornef M, Jäger M, Wagner H, Wolf H, & Schwarzmann F. (1997). Lytic Replication of Epstein-Barr Virus in the Peripheral Blood: Analysis of Viral Gene Expression in B Lymphocytes During Infectious Mononucleosis and in the Normal Carrier State. Blood, 89(5), 1665-1677. https://doi.org/10.1182/blood.v89.5.1665.
[15] Bajwah S, Wilcock A, Towers R, et al. (2020). Managing the supportive care needs of those affected by COVID-19. European Respiratory Journal, 55(4), 2000815. https://doi.org/10.1183/13993003.00815-2020.
[16] Lennon P, Crotty M, & Fenton J. (2015). Infectious mononucleosis. BMJ, 350(apr21 2), h1825-h1825. https://doi.org/10.1136/bmj.h1825.
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