Viruses: More Friends Than Foes (Revised Edition). Karin Moelling

“I got a cold”

      This is known to everybody; every winter we get seasonal flu, with fever, coughing, sneezing, aching joints and headache — often all at the same time. We should use some protection against sneezing, but hardly anyone still has a real handkerchief anymore. Paper tissues need to be used correctly — they should not go into a wastepaper basket, but into a bucket with a lid. Even on television it is now being demonstrated how should bend one’s arm and sneeze into the crook of the elbow.

      People should stay at home; otherwise, in no time at all, colleagues and people working on the same floor are going to become infected. In Switzerland I have always tried to avoid handshaking in clinical settings. However, as it is the western style of greeting and welcoming, but I was not allowed to omit the handshake, as it would have seemed unwelcoming and unfriendly. Yet now, handshaking has been abolished completely. Most respiratory diseases are transmitted by droplet infections, which can cover a distance of 50 cm and may transport 10⁵ virus particles in a single sneeze, and can be passed on via hands to others.

      “Getting a cold” is an apt description of how one can fall ill. Viruses become activated if our environment changes: a cold wind, wet clothes or wet shoes all affect our well-being, and they activate viruses. We live with the world of microorganisms in a balanced ecosystem, and we have an immune system that keeps viruses in check. Viruses do not have to seek us out: they are there all the time in our nose or throat, and all they need is the right conditions to make them virulent, which means start replicating. Dry air inside heated rooms, or outside frost, can increase viral activation and replication. Adults get two to four such infections each winter season, and children even more, with normally much higher amounts of viruses. They can easily infect their grandparents, whose immunity is reduced by ageing.

      Viruses select short distances. These are given in public transport, at mass events, in shopping malls or in schools.

      So far, this has been a description of any seasonal respiratory disease, such as occurs by viral infection in the autumn or the winter.

      The infection can be much worse if the cause is the real influenza virus. This is a very severe cold which starts quite abruptly with very high fever, pain and loss of consciousness. People suffering from it are too weak to get up.

      Another virus, different again, is the new coronavirus. It is called SARS-coronavirus-2 or CoV-2 for short. The disease is called COVID-19, an abbreviation of “Corona-Virus Infectious Disease from the year 2019” (the year when it first occurred). The term SARS refers to the first coronavirus, which went on the rampage in 2003, unleashing the first coronavirus pandemic that caused a “severe acute respiratory syndrome”, the symptoms of the atypical lung inflammation that it induced. Then there is a third member in this group of dangerous coronaviruses; it causes the “Middle East Respiratory Syndrome” (MERS) and first showed up in Saudi Arabia in 2012.

Many coronaviruses except for CoV-2

      Seasonal flus are recurring events every winter season. The viruses causing it are respiratory viruses and there are about 200 different ones. Seven of them are the most frequent ones: Rhinoviruses comprise 100 types, which make up about 30 to 50% of all colds. Then there are the four types of coronaviruses, which are harmless relatives of the three coronaviruses which caused the pandemics. They cause about 15 to 20% of the winter season infections. We tend to neglect them. It is not even known, whether they are related serologically to the new CoV-2 in respect to antibody response. Their names are HCoV-229E, OC42, NL63, and HKuV. The type 229E is related to the camel virus MERS. Furthermore, there is the respiratory syncytial virus (RSV) which is responsible for 15 to 20% of infections during winter. Others are Parainfluenza viruses, Enteroviruses, and in children the Metapneumovirus. Sometimes eye infections show up, which may be caused by Adenoviruses.

      Most of these viruses are single-stranded RNA viruses. As a consequence of the single-strands they can change rapidly, faster than double-stranded RNA or DNA viruses. The double-strand prevents changes, the mutations, and leads to more genetic stability of the viruses. Single-stranded RNA viruses can undergo rapid mutations, are innovative and escape from our immune response.

Other epidemics as models

      If there are new outbreaks, virologists or politicians have two possibilities: either to look into the history of virus epidemics or to look at other countries where the disease has progressed already — for CoV-2 that was China. Yet the virus was also new there. So the Influenza pandemic of 1918, the “Spanish Flu”, was studied carefully as potential model. The Spanish flu took off under extremely poor living conditions, crowded battlefields, a cold winter, poor sanitary conditions and famine. It cost the lives of 50–100 million people. It came in three peaks: the summer terminated the first peak and the Influenza disappeared, but it returned with the onset of winter, and this second wave surpassed the first one by far. A third wave came later and was again weak. This is the pattern which is in everybody’s mind now — the first wave may be over, but is there a much more dangerous second one still to come? Is this a valid model for COVID-19? That is the fear. We do not know. Also, we do not know whether CoV-2 is sensitive to summer temperatures like other respiratory viruses. During the northern summer, influenza viruses spread in the southern hemisphere, as it is winter there. Some CoV-2 has arrived there with some hot-spots of infection. Yet, the living conditions during the Spanish flu were poor and with present precautions we may prevent a second peak or face a weak one next winter.

      Models have been published about the course of the