Influenza or corona virus infection: Salicylate and lung hilum hyperthermia as inhibitors of disease progression during the incubation period *)

Günter Valet

SARS-CoV-2 infected patients (COVID-19) may suffer from severe respiratory problems and not recover despite high intensive care efforts (1). The observation of the author's flu episodes during the past 10 years was directed towards the identification of early intervention points within the incubation period of the viral infection sequence to inhibit potential disease progression towards pneumonia or severe acute respiratory distress syndrome (SARS, ARDS). Salicylate application in conjunction with lung hilum lymph node conditioning by temporary hyperthermia during the incubation period of influenza virus infections has reliably stopped typical disease outbreaks within the family environment without flu vaccination during the past 4 years, including two cases with beginning corona symptomatology (dry cough, dryness upper trachea and larynx) as well as two further cases with temporary loss of taste and smell in March 2020.

Symptoms like dry cough, altered tracheal and respiratory sensation, temporary anosmia, fatigue, as well as muscle and joint pain or skin and light hypersensitivity are observed during the respective incubation periods (37,3-37,9C body temperature (BT)). At the recognition of such symptoms, BT is determined to discriminate from non infectious (<37,3C) discomfort, followed by a 400mg effervescent aspirin tablet (only adults) as early symptom therapy and subsequently 3 or 4 tablets in 12 hour intervals (0-36/48h), totalling 1.6 or 2.0g of aspirin. Starting at the same time, local hyperthermia is applied to the lung hilus lymphnodes by drinking 4 cups (4x150=600ml) of 55-60C hot black or herbal tea in quantities between 10-20ml (half/full tablespoon) in continuous sequence to generate temporary retrosternal warmth. Smaller sips at higher temperature or larger quantities of lower temperature liquid do not generate the intended effect. It is recommended to start around 50C and to stepwise increase temperature according to individual tolerance to avoid thermal irritation of the oesophagus tissues. Tea drinking is continued at the subsequent time points (morning, noon or evening), followed by three hyperthermias per day (m, n, e) for 3-4 further days while the head and neck region is kept warm (cap, shawl).

Bronchial symptoms are significantly lowered within 3-4h after the first treatment and influenza disease will typically not break out. Cough decreases and disappears within a few days as well as a certain weakness of the circulatory system during physical work. Once the disease has broken out (typically >38C BT), salicylate, paracetamol or ibuprofen applications may attenuate symptoms but do not substantially influence disease course.

Despite the limited number of cases, it seems worth considering this inoffensive approach during the actual corona pandemia. The initial absence of humoral and cellular immunity (lympho-/monocytes, macrophages) against the SARS-CoV-2 virus in humans, leaves body defense in large parts to granulocytes and tissue macrophages. Granulocytes typically permeate blood capillary walls to phagocytize viruses and bacteria in lung tissue and alveoles where microorganisms are destroyed by diffusible reactive oxygen species like H2O2, molecular oxygen, hypochloric acid or enzymes such as myeloperoxidase or elastase. These effector molecules are likely to destroy bystander lung tissue, thereby preparing the ground for later superinfection by inhaled bacteria, viruses or fungal spores. Salicylates reduce granulocyte extravasation from the blood stream (2), thus lowering the early tissue damaging potential. At the same time granulocyte lifetime is shortened by accelerated apoptosis (3) and certain virus infections are inhibited (4). The remaining presence of granulocytes in the blood vessels provides higher intravasal virus phagocytosis capacity, thus potentially decreasing the extent of primary viremia during the virus incubation period. Primary viremia for influenza viruses is observed in mice (5) but not in human blood donors (6). Salicylates diminish in addition thrombocyte aggregability by irreversible cyclooxygenase blocking, thus counteracting the tendency for increased thrombus formation in COVID-19 patients (7). Hyperthermia in turn leads to lower virus replication in cells. This is partially due to a more efficient cellular antiviral response (8), and fever is accompanied by lower bacteria levels in patient blood (9). So as a tentative conclusion: Repeated temporary hyperthermias provide sufficient microorganism clearance in a structurally largely intact lung, which is less susceptible to bacterial superinfection despite salicylate induced lower granulocyte permeation into lung tissue and reduced granulocyte life span by accelerated apoptosis. Despite partial humoral and cellular immunity, the discussed sequence of events seems to equally prevail during influenza virus infections. Intensified efforts for individualized disease outcome predictions (10 table 4) might favor the early identification of risk patients, thus permitting timely adaptation of therapy, as long as the body has not crossed the recovery point. Patients beyond this point die at a certain degree of bacterial superinfection in case of therapeutic inactivity, but also upon massive application of antibiotics, probably from toxic products of destroyed microorganisms.

1. Thomas-Rüddel D, Winning J, Dickmann P, Quart D, Kortgen A, Janssens U, Bauer M. "Coronavirus disease 2019" (COVID-19): update for anesthesiologists and intensivists March 2020. Der Anaesthesist (2020) 69:225-235.
2. Spagnuolo PJ, Ellner JJ. Salicylate blockade of granulocyte adherence and the inflammatory response to experimental peritonitis. Blood (1979) 53:1018-22 .
3. Milot E, Filep JG. Regulation of neutrophil survival/apoptosis by mcl-1. TSWIJ (2011) 11:1948-62.
4. CJ Chen, SL Raung, MD Kuo, YM Wang. Suppression of Japanese encephalitis virus infection by non-steroidal anti inflammatory drugs. J Gen Virol (2002) 83:1897-1905.
5. Mori I, Komatsu T, Takeuchi K, Nakakuki K, Sudo M, Kimura Y. Viremia induced by influenza virus. Microb Pathol (1995) 19:237-44.
6. Stramer SL, Collins C, Nugent Th, Wang X, Fuschino M et al. Sensitive detection assays for influenza RNA do not reveal viremia in US blood donors. JID (2012) 205:886-94.
7. FA Klok, MJHA Kruip, NJM van der Meer, MS Arbous, DAMPJ Gommerse, KM Kant, FHJ Kaptein, J van Paassen, MAM Stalsa, MV Huisman, H Endeman. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020 in press
8. Foxman EF, Storer JA, Fitzgerald ME, Wasik BR, Hou L, Hongyu Zh., Tirner PE, Pyle AM, Iwasaki A. Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells. PNAS (2015) 112:827-32.
9. Weinstein MP, Towns ML, Quartey SM, Mirrett S, Reimer LG, Parmigiani G, Rell LB. The clinical significance of positive blood cultures in the 1990s: A prospective comprehensive evaluation of the microbiology, epidemiology, and outcome of bacteremia and fungemia in adults. CID (1997) 24:584-602.
10. Valet GK, Roth G, Kellermann Risk assessment for intensive care patients by automated classification of flow cytometric data. In: Phagocyte Function, Eds. JP Robinson, GF Babcock, Wiley-Liss Inc, New York 1998, p 289-306.

*) The above therapy concept was developed for family use. As consequence of the increasing severity of the current corona pandemia, it was made available on the Internet on March 30, 2020. It will hopefully decrease the number of diseased as well as of intensive care patients at a more widespread application.

© 2020 G.Valet
Last update: Oct 03,2020
First display: Mar 30,2020