faster than bacteria. Over subsequent chapters we shall see how that viral employment of host locomotion is one of many such evolutionary adaptations.
What then do rhinoviruses do when they get inside us?
We have seen that the rhinovirus has a specific target cell, the cilia-flapping cells lining the nasal passages. Once inhaled, the virus targets these lining cells, discovering a specific ‘receptor’ in the cell’s surface membrane, after which the virus uses the receptor to break through the membranous barrier and gain entry into the cell’s interior, or cytoplasm. Here the virus hijacks the cell’s metabolic pathways to convert it into a factory for the replication of daughter viruses. The daughter viruses are extruded into the nasal and air passages, there to search out new cells to infect and continue the invasive process. It seems to require only a tiny dose of virus to be inhaled from the expelled cough or sneeze of an infected person to initiate infection in a new individual. After arrival, the incubation period from virus entry to infected nasal cells exuding new daughter viruses can be as little as a day. We don’t have much of a chance of escaping infection once the virus has been inhaled. Virus replication peaks by day four.
Fortunately, it isn’t all one way. Even as the virus is launching its attack, the human immune system has registered the threat, and it has recognised the viral antigenic signature – what we call the serotype. The problem is that the arrival of a new serotype requires time for the immune system to recognise the threat and to build up a formidable arsenal of responses. By day six the nasal passages are the focus of a virus versus immunological war zone, with no quarter asked or given on either side. This intense immune response causes the nasal passages to shed most of their lining cells, exposing highly inflamed raw surfaces, with narrowed breathing passages exuding copious mucus, which contains rising levels of antibodies to the virus. The rhinovirus is eventually killed off by the neutralising antibodies and the ‘war detritus’ is cleared away by the gobbling action of phagocytic white cells. During this immunological conflagration the new host follows the same unfortunate cycle of being infectious to others, through coughing and sneezing, for a period of anything from one to three weeks.
There is an adage that colds will not kill you. This is largely true, but colds can make children more liable to sinusitis and otitis media, a nasty bacterial infection of the middle ear. Colds can also precipitate asthma in people constitutionally prone to it, and they can provoke secondary bacterial chest infections in people suffering from cystic fibrosis or chronic bronchitis. Nevertheless, the salutary consolation is that, in the great majority of human infections, the rhinovirus eventually passes on by and we make a complete recovery.
Is there anything we can do to minimise the risk of contracting that cold – or is there any effective treatment when we are afflicted?
In Roman times, Pliny the Younger recommended kissing the hairy muzzle of a mouse as a remedy for colds. Benjamin Franklin was more sensible, suggesting that exposure to cold and damp in the atmosphere was responsible for the development of a cold. He also recommended fresh air and avoiding the exhaled air of other people. More modern times have seen a veritable cornucopia of quack remedies for prevention or treatment of colds. One of the most popular was vitamin C, championed by the distinguished American chemist, Linus Pauling. But alas, when subjected to scientific scrutiny it proved no more effective than the mouse’s whiskers. Perhaps we should focus more on common sense? Colds are contracted from the coughs and sneezes of infected people. People in congested offices, or even relatives who find themselves ill at home, should follow the old adage: trap your germs in a handkerchief. If an individual is deemed to be at a particularly high risk from a cold, wearing a virus-level face mask would certainly reduce the likelihood of infection when exposed to an infectious source.
A pertinent question remains: why, then, if our immune system has come to recognise and react to the rhinovirus, are we still susceptible to further colds during our lifetime? In fact, there are roughly 100 different ‘serotypes’ of the rhinovirus, so immunisation to any one type would not provide adequate protection from the others. Added to this is the fact that serotypes are capable of evolving so that their antigenic properties are apt to change.
In 1994 the East African nation of Rwanda erupted onto the world’s news and television screens when a simmering civil war between the major population of Hutus and minority population of Tutsis erupted into a genocidal slaughter of the minority population. But despite the deaths of half a million Tutsis, the Hutu perpetrators lost the war, causing more than two million of them to flee the country. Roughly half of these fled northwest, across the border of what was then Zaire, these days the Democratic Republic of the Congo, where they ended up around the town of Goma. Up to this point Goma had been a quiet town of some 80,000 people, nestling by Lake Kivu in the lee of a volcano. Goma now found itself overwhelmed by a desperate torrent of refugees, carrying everything from blankets to their meagre rations of yams and beans. Two hundred thousand arrived in a single day, confused, thirsty, hungry and homeless. They camped on doorsteps, in schoolyards and cemeteries, in fields so crowded that people slept standing up. Agencies from the world’s media flocked to the vicinity, reporting the chaos and the urgent need for shelter, food and water.
A reporter for Time magazine estimated that the volume of refugees needed an extra million gallons of purified water each day to prevent deaths from simple thirst, meanwhile the rescue services were managing no more than 50,000. Desperate people foraged for fresh water, scrabbling hopelessly in a hard volcanic soil that needed heavy mechanical diggers to sink a well or a latrine. Human waste from the relief camps fouled the waters of the neighbouring Lake Kivu, creating the perfect circumstances for the age-old plague of cholera to emerge. Within 24 hours of confirmation of the disease some 800 people were dead. Then it became impossible to keep count.
Viruses are not the only cause of plagues, which include a number of lethal bacteria, such as the beta-haemolytic streptococcus, tuberculosis and typhus, as well as some protists, which cause endemic illnesses such as malaria, schistosomiasis and toxoplasmosis. Cholera is a bacterial disease, caused by the comma-shaped Vibrio cholerae. The disease is thought to have originated in the Bengal Basin, with historical references to its lethal outbreaks in India from as early as 400 CE. Transmission of the germ is complex, involving two very different stages. In the aquatic reservoir the bug appears to reproduce in plankton, eggs, amoebae and debris, contaminating the surrounding water. From here it is spread to humans who drink the contaminated water, where it provokes intense gastroenteritis, which proves rapidly fatal from massive dehydration as a result of the fulminant ‘rice-water’ diarrhoea. This human phase offers a second reservoir for infection to the bug. If not prevented by strict hygiene measures, the extremely contagious and virulent gut infection causes massive effluent of rice-water stools that are uncontrollable in the individual sufferer, so that they contaminate their surroundings, and especially any local sources of drinking water, leading to a vicious spiral of very rapid spread and multiplication of the germ.
During the nineteenth century, cholera spread from its natural heartland, provoking epidemics in many countries of Asia, Europe, Africa and America. The massive diarrhoeal effluent of cholera is unlike any normal food poisoning. An affected adult can lose 30 litres of fluid and electrolytes in a single day. Within the space of hours, the victims go into a lethargic shock and die from heart failure.
The English anaesthetist, John Snow, was the first to link cholera with contaminated water, expounding his theory in an essay published in 1849. He put this theory to the test during a London-based outbreak around Broad Street, in 1854, when he predicted that the disease was disseminated by the emptying of sewers into the drinking water of the community. Snow’s thoughtful research led to the civic authorities throughout the world realising the importance of clean drinking water.
