I found this article in the April 13, 2020 issue of The New Yorker to be very informative about why fighting viruses is so much harder than fighting bacterial infections, especially those viruses like Covid-19 with a genome of RNA, because they evolve faster than those with DNA.
Furthermore while we have antibiotics that are effective against a whole array of bacterial infections, viruses require specialized, highly targeted treatments and we do not have them for most viruses. What is most effective against viruses are vaccines to prevent the onset of the disease. At the moment we do not have an antiviral drug effective against Covid-19 nor do we have a vaccine. Since these viruses also mutate easily, a treatment and vaccine that is developed for one may not work against the next virus that comes along. This is the same problem faced with flu vaccines, where they cannot be sure what type of virus will emerge the next year.
None of our off-the-shelf treatments equip us for such a pandemic. If bacteria invade, there’s a long list of antibiotics you can try. Between ciprofloxacin and amoxicillin, we can treat dozens of different types of bacterial infection. For the roughly two hundred identified viruses that afflict us, there are approved treatments for only ten or so. And the antiviral drugs that exist tend to have narrow targets. Only a few have been approved for use against more than one disease. Many drugs that work on one virus don’t work on others within the same family; antivirals suited for some herpesviruses (such as the one that causes chicken pox and shingles) aren’t suited for others. Some antivirals can’t even treat different strains of the same virus.
The most valuable weapon against viruses remains the vaccine—but vaccines (at least the kinds we’ve formulated so far) tend to work against only specific, identified viruses, and have to be taken before infection. Since they’re not effective for everyone, moreover, we’d want antivirals for acute treatment even if we had a vaccine in hand. And fast-mutating viruses, like influenza, present a moving target, which is why, by the time a new batch of flu vaccine is manufactured every year, it’s already outdated, powerless to fight much of what comes along. These limitations typically apply to antibody therapies as well: they tend to be specific to a single, already encountered virus, and can’t be stockpiled for use against new ones.
This transient nature of viruses makes the private sector reluctant to get involved in developing vaccines and drugs to combat them since they are not guaranteed of long-term sales. The responsibility falls on governments and the entities they fund like research universities and institutes to do this work.
Given all these difficulties, this is why preventing the spread of the virus by social distancing and other means is the most effective tool that we have at present to curb this pandemic and we should expect to do this again when the next pandemic comes along. Even before that, there is a danger that there might be a second wave of this same virus as restrictions are relaxed. China and South Korea are the nations to watch in this regard. They seemed to have stopped the first wave and are easing up on social distancing. If the virus returns there, that should alert the rest of the world to this danger.
Dr Akiko Iwasaki, professor of immunology at Yale University, and Dr Julia Marcus, infectious disease epidemiologist at Harvard Medical School, answer some common concerns about how long the virus can survive on surfaces, how many particles it might take to become infected, and what precautions can or need to be taken when handling groceries and other packages to prevent the spread of the virus.
On an encouraging note, I notice that the infectious growth line is starting to curve downward for many countries. If you look closely, even the US seems to be showing the tiniest sign of deviation from the exponential growth curve.