A blog post for the non-expert
Our best hope against Covid-19 is an effective vaccine, and efforts in that direction are galloping along like no other time in history. There are so many vaccines being investigated, it’s hard to keep up with the numbers, but at the time of writing there appear to be well over 100, with around 40 in active clinical trials. Despite a lot of dangerous nonsense circulating the internet that Bill Gates wants to control our DNA through microchips implanted via vaccines, in reality they are without doubt the most successful weapon in humankind’s fight against infectious disease. The adage that vaccines “prime the immune system against infection” hides an incredible biochemical complexity, that’s truly mind-blowing. If you want a simplistic, but more accurate description of what a vaccine does, I’d describe them as “interjecting into the body’s biochemistry to up-regulate the immune system against an infecting organism”. More accurate perhaps, but, I’ll grant, less catchy.
It’s undoubtedly true, Covid-19 is likely to remain as disruptive and destructive as ever, until one, or more, of those vaccines comes through. In the meantime however, scientists are also investigating drug-based approaches to alleviate symptoms and save the lives of those infected. Now and again one of these drugs, such as dexamethasone hits the headlines but there’s one reported recently, albeit behind the headlines, which, like a vaccine, interjects into the complexity of the immune system to exert its therapeutic effect – and that’s interferon.
As ever, we have to be cautious of the claims because so far we only have a press release (I blogged on science by press release previously) but interferon is currently used to treat, for example, viral infections in asthma patients and so does have an established track record. There are two sides to understanding the effectiveness of any drug, the mechanism by which it works, and to what extent it improves patient recovery. Let’s look at the mechanism first.
Interferon is a protein, and since I’ve blogged on the complexity of proteins before, I’ll not repeat it here. There are three types of interferon, alpha (α), beta (β) and gamma (ɣ), but the one of interest here is β-interferon. It comprises 166 amino acids along with attached sugars (see image). In the immune army, interferon belongs to the signal corps. As viruses attack, cells release interferon sounding a warning bell to other cells that a virus is on the rampage. Cells receiving the message switch on genes to up-regulate antigen presentation, which essentially means they present the immune system with something to attack. Antibodies are then made against the antigen, which place flags on the viral particles for an army of white cells to attack and destroy. All well and good, but some viruses have evolved ways to block interferons, like jamming the signal corp’s radios so they can’t communicate. The virus causing dengue fever, for example, is well known for this assault on interferon and there’s evidence SARS-CoV-2 can do something similar. Introducing additional β-interferon directly into the lungs through a nebuliser, so the hypothesis goes, restores the balance and the signals can get through once more.
The theory appears sound, but how effective is β-interferon against Covid-19 in practice? Evidence to date comes from a single study of 101 patients randomised between those receiving β-interferon (code named SNG001) and those receiving a placebo. The study was conducted by Synairgen plc who reported patients receiving β-interferon were, on average, released from hospital 3-days earlier than those on a placebo. Recovery over 28-days was almost four-times higher with β-interferon although it had little effect on the death-rate. The key findings are in the company’s press release.
Media emphasis has been on Covid-19 death rates but the virus also causes much suffering and leaves some survivors with significant medical problems. Until an effective vaccine does come along, drugs such as β-interferon and aforementioned dexamethasone, which at first sight may seem to have limited efficacy, nevertheless have a potentially important role in the fight against the most severe symptoms. There are also other drug regimens emerging, such as administration of multiple therapies. One recent study looked at combining β-interferon with ritonavir and ribavirin, for example.
As cells receive interferon’s viral distress call, it can induce flu-like symptoms, which on top of those of Covid-19 is certainly problematic. But small steps are welcome during a pandemic and it nevertheless gives reason for optimism.