Viruses are obligate intracellular parasites; in other words, they rely on the host cell for replication. Without those they have just invaded (infection) they can’t function or “live”.
So, are viruses alive?
The problem is that we think of things as alive or dead. Are people alive, silly question, if they’re breathing, they are, right? What about plants – are they alive, yes, we accept they are even if through the inactive ‘seed’ stage.
Bacteria – yes. They’re either active or not. That doesn’t mean that you’ll get sick (show signs and/or symptoms of being infected) because as we know our ability to fight an infection (our “immunity”) is an important part of the puzzle.
Viruses are different, they can be alive, and “work” their damage, but they’re dead because they’re using you, or their host to live. The problem is then, if they’re not living – how do you kill something that’s dead already?
How do viruses work?
Unlike other species, viruses can’t reproduce on their own. They need to infect or invade a host cell. Again, they are obligate intracellular parasites that make the host cell do all the work to duplicate the virus.
Viruses don’t “respond”. You can’t poke them or set up barriers, it doesn’t matter, in that respect they seem “dead” but they’re either active or inactive based on whether they’re doing something or not. They are either potentially functional or they are destroyed, because again, how could you kill them if they’re not alive?
What are viruses made up of?
Viruses don’t really have any cells or organs. While there some advanced viruses most don’t have any of the parts you would normally find in any other cell. They have no nuclei, mitochondria, or ribosomes. Some viruses do not even have cytoplasm, the active cell “filler”.
Viruses do have a few basic components. The most important part is a small piece of DNA or RNA (never both), in COVID-19 its RNA. That strand of nucleic acid is considered the core of the virus – it’s the ‘virus’ genome, the bit that the virus will have the host duplicate.
Such an active replication of the viral ‘genome’ results in cell destruction or “lytic infection” characterized by the release of new progeny virus particles, often upon this lysis of the host cell.
Inactive or latent Viruses
Another mode of virus infection is the latent phase, where the virus is ‘quiescent’ (a state in which the virus is not replicating), the virus is still potentially active, but appears, well, dead. It’s believed that COVID-19 may have “reactivated” in some people in South Korea, as opposed to them being re-infected all over again, or that repeat testing may simply be picking up harmless fragments of virus genetic material that can linger for weeks or months after a person recovers.
A combination of these stages, where virus replication involves stages of both silent and productive infection without rapidly killing or even producing excessive damage to the host cells, falls under the umbrella of a “persistent infection.”
Viruses are known to cause latent infections, this includes, herpes simplex virus, varicella zoster virus, Epstein–Barr virus, human cytomegalovirus, human herpesvirus 6, human herpesvirus 7, Kaposi’s sarcoma-associated herpesvirus associated with AIDS, JC virus, BK virus, parvovirus and yes, adenovirus.
Re-activation of viruses
Reactivation is the process by which a latent virus switches to a lytic phase of replication. Reactivation may be provoked by a combination of an external and/or internal stimulus from the host cell. Understanding this mechanism is essential in developing future therapeutic agents against viral infection and subsequent disease – the problem is that right now, with COVID-19, we don’t know.
COVID-19 is unlike most that capture popular attention, it is deadly, but not too deadly. It’s contagious and can make people sick, but not in predictable, uniquely identifiable ways— COVID-19 may be most dangerous because, it seems, it may sometimes cause no symptoms at all.
The majority of the world’s population becomes infected with multiple herpesviruses during childhood, and after clearance of acute infection, viral latency is established in the host and persists for life. On one hand, latency is deemed a beneficial symbiotic (immunity) relationship, but to this notion’s detriment, it can be considered that viral persistence in latent phase is the greatest obstacle for effective antiviral therapy. With COVID-19, chances are, somewhere along the way, you’ll be exposed to it, get it, and recover from it.
Reactivation from viral latency is associated with an array of human pathologies. Although normally controlled in immunocompetent adults, β-herpesvirus, CMV, can cause severe disease such as hepatitis following reactivation in immunosuppressed hosts. VZV, for example, can reactivate from its latent state to cause shingles/zoster in the adult. Viruses don’t always work the way that other parasites work. What’s the point in killing your host – but then, it’s not the virus that kill, it’s the consequences.
Vaccines for viruses
To date, virus vaccines are completely ineffective during latency; only upon reactivation to lytic phase are current vaccines beneficial treatments, there is no obvious solution of how to destroy herpesvirus DNA concealed in latently infected cells, as latent viruses are unaffected by any of the conventional nucleoside analogs or drugs that rely on viral protein targets.
Although vaccination against herpes viruses has been difficult, advancements have been made; in fact, HSV was among the very first infections to be treated successfully using antiviral compounds, proving that a viral disease could be successfully treated in this way.
With COVID-19, we don’t know and despite our ability to determine how to do so (using genetic coding) it’s likely to be 12-18 months before we’ve got one and even then, it won’t eradicate the disease, just infer some protection.
Will COVID-19 disappear eventually?
Many virologists consider that it will just remain with us and we’ll get “flu season” and “COVID season”, that is, we’ll never achieve true containment or eradicate the virus or potential for disease, just like smallpox, polio, measles, etc.
Recovery from COVID-19 may be in large part due to effective immune response. With SARS and MERS viruses, natural immunity to these viruses is short-lived. In fact, some animals can be reinfected with the very same strain that caused infection in the first place.
One prominent COVID-19 vaccine candidate is based on RNA (its core), which the virus uses as its genetic code; although it’s unproven as yet, but we don’t know which vaccine type will work—and the best strategy is to try them all, mounting a massive effort that is already underway.
Now there are conflicting reports on whether the new coronavirus can remain viable for a long time in an aerosol – studies suggesting that it can be aerosolized are only preliminary, and other research contradicts it, finding no aerosolized coronavirus particles in the hospital rooms of Covid-19 patients.
The weight of the evidence suggests that the new coronavirus can exist as an aerosol under only very limited conditions, and that this transmission route is not driving the pandemic. This was a concern in dentistry that produces aerosols (both in fillings and cleanings).
However, “limited” conditions does not mean “no” conditions, underlining the need for health care workers to have high levels of personal protection, especially when doing procedures that have the greatest chance of creating coronavirus aerosols.
Viruses have protein and that’s why certain actions like (high) heat can “denature” or inactivate them. So, my take is this, prevention of cross infection is our best hope because COVID-19 can only be “caught” while it’s active.
That’s why hand washing is important, as although it’s still possible to contract coronavirus from touching your face with virus-contaminated hands, you can also catch it directly from the coughs or sneezes of an infected person. So, while washing your hands won’t eliminate your risk of infection completely, it’s a sensible and effective safety measure like wearing a seat belt in a car.
TA viruses coat – their important weakness.
They also have a protein coat to protect the nucleic acid. That coat is called the capsid which COVID-19 hasn’t got. The capsid protects the core but also helps the virus infect “hosts”. Some viruses have another coat or shell called the envelope which is made of lipids (fats) and proteins in the way a regular cell layer or membrane is structured. This envelope can help a virus get into systems unnoticed and then help them invade new host cells.
Washing your hand’s with soap and water
This coat may also be their Achille’s Heel, it’s this lipid coat that can be disrupted with alcohol, salt , soap or other disinfectants. While there’s no evidence that nasal lavage (rinsing with saline) works to protect the individual, there is strong evidence that soap disrupts the coat as does salt and a number of other substances (soap, alcohol, bleach) so ocean water is likely safe.
Denaturing virus protein
Viruses have protein and that’s why certain actions like (high) heat can “denature” or inactivate them too. So, my take is this, prevention of cross infection is our best hope because COVID-19 can only be “caught” while it’s active.
Prevention of cross infection is our first line of attack; vaccination may be very useful. Innate immunity may play a role as will genetic protection. Increasing our immune systems makes very good sense against any potential pathogen although there are no guarantees in life.
Long-term planning makes sense, as we may be living with this as a long-term infective agent. Hand washing with soap and water is worthwhile. Skincare is also beneficial in order to main the integrity of this protective surface (skin) to the body too.
Stephen Bray May 2020