Virolution. Frank Ryan
Читать онлайн книгу.
of tiny carcasses – bats with their wings extended to full stretch, and rodents, tens of thousands of tiny bodies, all neatly arranged, from whiskers to tautly stretched tails. The collection was not merely exhaustive in numbers, it was also comprehensive in time, dating back to the 1880s when naturalists had accompanied the new railroads out west. Hidden away in those myriad rows of cupboards, with their meticulously tagged corpses, lay the answer to the emergence of the plague outbreak.
Those extreme circumstances began on 14 May 1993 with an ambulance screaming westwards through the dry desert roads of New Mexico, heading for the Indian Health Service Hospital in Gallup. The ambulance crew had radioed ahead so that, as the ambulance reversed back into the admissions bay, the emergency medical staff, under the direction of Dr Bruce Tempest, were already waiting by the entrance to lift the occupant, a young Navajo male, onto a gurney and rush him to the emergency area, where he was subjected to an emergency chest x-ray even as cardiopulmonary resuscitation began. The chest x-ray showed a bizarre picture – instead of the normal, slightly feathery transparency of healthy lungs, the young man’s chest showed a solid opaque white. The air sacs had been flooded with some pathological process, whether fluid or pneumonic exudates, leaving no room at all for air to get through. In effect, he was drowning in his own body’s secretions. Resuscitation was unsuccessful and the young man was pronounced dead right there in the emergency room.
In such tragic circumstance arrived a new or “emerging” plague into the Four Corners States of New Mexico, Arizona, Utah and Colorado. Although it began in the territory of the Navajo Nation, it soon manifested in the non-Navajo areas of the other states, and spread far and wide throughout the rest of America. But the epicentre was always focused on the desert areas of New Mexico and Arizona, where it terrified the local community, often infecting previously fit young people who could be reduced from rude good health to death, with whited-out lungs, in 24 hours. When I first arrived in New Mexico, the plague was still rampant, with the entire intensive care unit at the University Hospital in Albuquerque devoted to looking after newly diagnosed cases. Through intensive modern investigation and devoted medical management by the medical staff in various cities and hospitals, the death rate had been clawed back from an initial 70% to something closer to 50%. My purpose in coming to New Mexico was to examine new, or “emerging plagues”, and particularly those caused by viruses, such as Ebola and HIV-1, as part of the researches for my book, Virus X,5 and so the emergence of this all-American plague afforded me a rare opportunity to examine the most intensive modern medical and scientific response, in day-to-day detail. I found that the investigation of the plague, and the medical management of its victims, was still at its height, and I was duly grateful to my hard-pressed and dedicated colleagues, who allowed me to sit in with them in their clinical meetings and scientific experiments.
I knew that scientists working in the Special Pathogens’ Branch of the Centers for Disease Control in Atlanta – the world-famous plague hunters – had discovered that the Four-Corners’ epidemic was caused by a hitherto unknown virus. Here then was the opportunity to see for myself where such emerging viruses came from in nature, and why they behaved as aggressively as they so often did when they encountered a new host, such as our human species. In Albuquerque I would spend some time observing the doctors in the University Hospital, fighting to save the lives of infected patients. Here they did me the great courtesy of allowing me to interview victims and their relatives, with the normal medical confidentiality, and to witness for myself the harrowing experience of contracting an emerging plague virus. I travelled to Atlanta to observe the work of the virologists and geneticists at the Centers for Disease Control, where they had first realised that they were dealing with a newly emerging virus, which was a member of the genus of viruses known as the “hantaviruses”, using molecular techniques only 13 days after the onset of the epidemic. It took them six more months to see the actual virus, which would subsequently be called the Sin Nombre hantavirus – the hantavirus with no name. I sat in on the online discussions between the virologists and the epidemiologists at CDC and the internists and medical investigators in Albuquerque. I found myself gazing with curiosity at images of the new virus taken with the electron microscope, which looked as innocuous as minuscule balls of cotton wool. I moved on to California, where I interviewed virologists who had investigated the first African outbreak of Ebola and who had been intimately involved with the investigation of the emerging virus we now know as HIV-1, the cause of the AIDS pandemic. It was towards the end of my exploration of the Sin Nombre outbreak, and after I had collected a great many interviews with the scientists investigating it, that I returned to Albuquerque to talk toTerry Yates, one more interview as I supposed among many, when I wanted to look at what the biologists had discovered about the animal source of the virus.
I knew by then that the virus that was so lethal in people had come from the commonest rodent in America, the humble deer mouse, the equivalent of the common field mouse back in the UK. And in that conversation, I sensed the ground shift beneath my feet, as I listened with a growing astonishment to the slightly built and dark-haired Yates as he explained, with a fast and engaging Kentuckian accent, his own take on plague viruses, and hantaviruses in particular.
In addition to his chair in zoology, Yates was also the director of an important biological field reserve in New Mexico, known as the “Sevilleta”, where biologists are conducting one of the most comprehensive ecological surveillance programmes in history. This, in major part, is where the gigantic collection of mammals in the museum has come from. Yates was a world-famous expert in mammalian evolution. He did not focus, as most biologists do, on a single species or even a genus. His interest lay in evolutionary systematics: in the patterns and processes that lead to the diversity of animal species and how this gives rise to the branching tree of their evolution. The outbreak of the Sin Nombre hantavirus epidemic in his own back yard added a new, and unforeseen, practical significance to the theoretical work he and his team had been engaged in for decades. Not only could Yates and his fellow scientists look for the hantavirus in living deer mice, but they could also extract viral sequences from the vast trawl of carcasses stored in the museum and from there they could trace important facts about the virus’ own evolution. What then, I ventured to ask him, was the ultimate purpose of this exercise?
‘We’re interested,’ he told me, ‘in the co-evolutionary potential of the hantavirus as it evolves in direct parallel with the host.’
His reply surprised me. Like most doctors, I thought of viruses as nothing more than parasites. I was taught modern Darwinian evolution as part of the core biology that underpins our understanding of medicine. Lay people often confuse viruses with bacteria but they are radically different organisms. Most viruses are a lot smaller than bacteria, so small in fact that most are completely invisible even under the highest magnifications of the light microscope. Only through more subtle detective work, using immunological probes, or molecular chemistry, or, ultimately, the vast magnification of the electron microscope, can we bring them into focus. In their genetic arrangements viruses also differ markedly from bacteria. Their DNA is usually packaged in the linear clusters we call genes, rather like our own, while the DNA of bacteria is packaged in a single ring. Viruses are also the ultimate masters of evolution through mutation. They mutate with astonishing speed, something like a thousand times faster than bacteria, which in turn mutate approximately a thousand times faster than we do. Mutation of this order is an important consideration for medicine since it is one of the ways in which bacteria and viruses become resistant to antibacterial and antiviral drugs. For example, it is the key to understanding resistance to therapy in conditions such as AIDS and tuberculosis, where the phenomenal mutational capacity of the HIV-1 virus and the tuberculosis bacterium means that we are obliged to prescribe a cocktail of different drugs to control them.
In this conversation with Terry Yates, I discovered that many different species of rodents around the world appeared to have hantaviruses that infected them. The first hantavirus ever discovered came from a rodent in Korea – it emerged close to the Hantaan River, which gave its name to the genus of viruses as well as to the human illness the virus caused, which is known as Hantaan fever. So when Yates told me he was looking into the evolutionary aspects of the hantaviruses, I presumed that he was talking about mutation. I knew nothing about the co-evolution of a virus in parallel with its host. Indeed, I was still thinking along the conventional medical and evolutionary lines when I asked him another question.