COVID-19 — basics

1. COVID-19 — basics

COVID-19 (Coronavirus Disease 2019) is the illness caused by the virus SARS-CoV-2. This section summarises virology, course, acute complications, risk groups, the current variant situation and vaccination in an evidence-based way, and places their relevance for Long COVID in context.

What is SARS-CoV-2?

SARS-CoV-2 belongs to the Coronaviridae family, genus Betacoronavirus (subgenus Sarbecovirus). It is an enveloped virus with a single-stranded positive-sense RNA of around 30,000 bases – one of the largest known RNA virus genomes [3]. Four structural proteins make up the virus particle: spike (S), envelope (E), membrane (M) and nucleocapsid (N) [3].

The way it enters cells explains the multi-organ character of the illness: the receptor-binding domain (RBD) of the spike protein's S1 subunit binds to angiotensin-converting enzyme 2 (ACE2) as its cell receptor. The serine protease TMPRSS2 and furin (at the S1/S2 cleavage site) "prime" the spike and enable membrane fusion [2]. Because ACE2 and TMPRSS2 are present in the epithelium of the airways, heart, kidney and gut (and in part in the vascular endothelium), the virus can affect several organ systems [2].

Symptoms and course

Typical acute leading symptoms are fever, dry cough, sore throat, fatigue/exhaustion, muscle pain (myalgia), headache, shortness of breath (dyspnoea) and nausea/diarrhoea. The variant-dependent loss of smell and taste (anosmia/ageusia) occurred above all in the pre-Omicron period [1]. The incubation period is a median of about 5 days, and for Omicron more like 3–4 days [1].

The following severity classification per NIH/WHO is a clinical grading tool (not intended for self-diagnosis or self-treatment) [1]: - asymptomatic: infection without symptoms - mild: symptoms without shortness of breath or abnormal imaging - moderate: lower airways affected, oxygen saturation (SpO2) ≥94 % on room air - severe: SpO2 <94 %, respiratory rate >30/min, PaO2/FiO2 <300 mmHg or lung infiltrates >50 % - critical: respiratory failure, septic shock, multi-organ dysfunction

Warning: In the event of shortness of breath, persistently low oxygen saturation, chest pain, confusion or a bluish-grey discolouration of the lips/skin, seek medical or emergency help (emergency call) immediately. The limits given do not replace a doctor's assessment.

Mortality depends strongly on age. The infection fatality rate (IFR) values given here come from a meta-analysis from the early pandemic phase (Levin et al. 2020, before broad immunity from vaccination/infection and before Omicron) [4]: roughly ~0.01 % at age 25, ~0.4 % at 55, ~1.4 % at 65, ~4.6 % at 75 and ~15 % at 85 – the IFR rises approximately log-linearly (doubling roughly every 5–8 years of life). Around 90 % of the geographic IFR differences were explained in this analysis by age structure alone [4]. Important: these historical IFR values cannot be carried over to today's situation; because of vaccination, past infections and less virulent Omicron sublineages, the current IFR is considerably lower. The age dependence as such, however, remains.

Acute complications

• Lungs: viral pneumonia and acute respiratory distress syndrome (ARDS) are the main reason for intensive care; imaging shows bilateral, peripheral ground-glass opacities. Severe courses require oxygen up to invasive ventilation [1].
• Heart: myocardial damage (raised troponin) is found in about 20–25 % of all hospitalised patients, and higher in severe courses; cardiac arrhythmias (above all atrial fibrillation) in up to ~10 %, acute myocarditis rarely (on the order of a few per 1,000 hospitalisations). These frequencies vary considerably depending on study, population and time of assessment. Myocardial damage is associated with markedly increased in-hospital mortality [5].
• Clotting: the COVID-associated coagulopathy (raised D-dimer) favours venous thromboembolism (deep vein thrombosis, pulmonary embolism), especially in intensive care. This is why standard thrombosis prophylaxis is given to hospitalised patients (medically indicated and monitored — not self-medication) [7].
• Kidney: acute kidney injury (AKI) affects roughly ~10 % on a normal ward up to 30–45 % of intensive-care patients; some become dialysis-dependent. AKI is strongly associated with increased mortality and longer length of stay [6].

Risk groups

The strongest risk factor for a severe course is higher age, followed by male sex, obesity, diabetes mellitus, arterial hypertension/cardiovascular pre-existing conditions, chronic lung (COPD) and kidney diseases, immunosuppression and pregnancy [1][4].

Variants (as of 2026)

Note on timeliness: virus variants and their WHO classification change continuously. The following details are time-sensitive and should, before use, be checked against the current lists from WHO, ECDC and RKI.

As of this section there are no more official Variants of Concern (VOC). Only Omicron sublineages are circulating; among the Variants of Interest or Variants under Monitoring were, among others, the BA.2.86 lineage, XFG, NB.1.8.1 and BA.3.2 — each without solid evidence of increased disease severity [8][9]. (The exact classification — VOI vs. VUM — and which lineage currently dominates must be checked against up-to-date sources.) Earlier main lineages were Alpha, Beta, Gamma, Delta and the earlier Omicron waves (BA.1/BA.2/BA.5, later JN.1).

Vaccination

The vaccines of the 2025/2026 season adapted to JN.1/LP.8.1 reduced emergency-department visits by ~50 % and hospitalisations by ~55 % in CDC studies (in those aged ≥65, ~48 % and ~53 % respectively) [10][11]; European VEBIS data showed ~59 % protection against medically attended illness (95 % CI 14–83 %), with protection waning over time [10]. The German STIKO recommends an ongoing booster, adapted each year to the circulating variant, above all for risk groups: those aged ≥60, chronically ill/immunocompromised people, nursing-home residents, medical staff and close contacts of the immunocompromised [10]. Safety note: vaccines are approved medicines; individual indication, benefit and possible side effects should be discussed with a doctor. The efficacy figures given are observational data (not randomised trials) with in part wide confidence intervals and apply to the respective period/population studied.

Relevance for Long COVID / ME-CFS

Especially important for this platform: post-COVID states including post-exertional malaise (PEM) and an ME/CFS phenotype can occur even after a mild acute course. The risk tends to be higher with a severe course, but is not limited to it [12][13]. If PEM is present as a core symptom, pacing/energy management is indicated; forced activation or a graded exercise therapy (GET) oriented towards increasing performance can be harmful in PEM and is not recommended as standard therapy for those with PEM in current guidelines (e.g. NICE 2021) [12][13].

This text serves as information, does not replace medical advice and contains no individual healing or treatment instruction. It makes no promise of a cure. Where uncertainties exist (e.g. wide confidence intervals, population-dependent frequencies, historical or time-critical data), they are flagged. The source references [1]–[13] named in the text have not yet been built out into their own clickable reference list for this chapter (unlike, for example, chapter 12), and could not be looked up individually within this review. For questions about specific figures: hallo@mypacing.app.