A Blast from the Past

A hot button microbe right up there with MRSA, I’m sure nearly every one of us is mindful of Human Immunodeficiency Virus or HIV. HIV has found our Achilles Heel, as it targets the very cells we trust to protect us from invading microbes and viruses such as itself. But the ingenious of this virus is beyond even these tactics, as HIV is a retrovirus.

This designation does not simply mean that HIV is keeping it fresh with style from the 70s, but rather that HIV has some sweet dance moves that can turn everything we thought we knew on its head!

Retroviruses fall within the virus family, Retroviridae, and typically have a single strand of RNA as their genetic blueprint. While RNA genes instead of DNA genes might seem strange for cellular life, viruses bend the rules a bit. In other words, it is not rebellious for a virus to chose RNA rather than DNA; in fact, it is quite hip. HIV acts as a typical RNA virus, dormant and zombie-like until it snags its favorite flavor of cell surface protein. And just as soon as HIV finagles its way inside its new host, is when the magic happens. The ace hidden up HIV’s sleeve is an enzyme known as RT or reverse transcriptase. As hinted by its name, this is the enzyme that turns the beat around!

Reverse transcriptase begins by taking the single strand of viral RNA and using it to fashion a new strand of DNA. But hold up: this seemingly innocent process is actually quite the stunt! In biology, DNA is used to make RNA, not the other way around. But since reverse transcriptase doesn’t seem to subscribe to the “save the best for last” mentality, it pulls this showstopper seemingly from nowhere. This opening trick, leaves one strand of RNA and one strand of DNA in a hybrid molecule of sorts. This is definitely something you don’t see every day, but if you blink you might miss it, as reverse transcriptase keeps the show entertaining by making the RNA strand disappear.

But RT is a performer of many talents, so it wraps up with a spectacular finale: crafting a new DNA strand from the lone DNA strand to fashion a double-stranded DNA molecule.

And just like that, the magnificent reverse transcriptase has transformed one measly strand of RNA into two DNA strands. But besides the wow-factor, why would HIV want this spectacle? I mean, RNA viruses can replicate themselves perfectly adeptly without reverse transcriptase. The secret that answers this inquiry is that this double-stranded DNA molecule is a clandestine operative that sneaks into a host chromosome and implants itself. Reminiscent of a “prophage,” this viral spy is known as a “provirus” and lays low until it is activated. The provirus unwinds itself and proceeds with copying itself and building new virus particles as any other RNA virus.

This show is full of awe-inspiring surprises, but also chock full of implications. For one, antivirals are few and far between, as when viruses replicate, they use enzymes and machinery from a host cell, and we do not want to inhibit something that might hurt our own cells. But reverse transcriptase is specific to retroviruses such as HIV. This means that even though RT is HIV’s secret agent, it is also its Achilles Heel. AZT is a potent inhibitor of HIV replication as it is able to grab onto and block its reverse transcriptase.

Either way, reverse transcriptase and retroviruses are super fascinating!

Beware the Cooties!

I thought we had left “cooties” behind in elementary school, but they’re making a repeat appearance nearly 15 years later in college!

 

Photo by Ed Uthman.

But, of course, these cooties are none other than the “kissing virus,” Mono, itself. And Epstein-Barr Virus or EBV, the tiny tyrant behind Mononucleosis, is astoundingly widespread. According to the CDC, nearly everyone has a run in with EBV at some point in their lives. In fact, 85% of 40-year-old United States residents have already been infected with EBV. It just happens to be that EBV infection in childhood is frequently asymptomatic. In other words, this infection might have snuck past us in childhood.

When it comes to our friendly, neighborhood rhinoviruses, it turns out that you can never suffer through the same cold twice! Our immune system learns from its mistakes; if it has already had to fight a specific microbe before, it keeps a few antibodies hanging around so that it can effortlessly spot and eradicate a repeat offender even several decades later. Talk about an impressive memory! But for EBV it is quite the opposite; you never seem to quite get rid of it.

EBV is a herpesvirus, a family notorious for viral latency. When EBV becomes latent, it just fundamentally comes to be that mooching roommate that seems to be constantly asleep. If you don’t take a close enough look, you might miss it! In latency, the virus slips an entire copy of its blueprints into the DNA of one of our cells but keeps itself under such tight lock and key that no more than a few viral proteins can be produced, not to mention an entire viral particle! But EBV can only stay under the radar behind enemy lines for so long; instead, it often rebounds and comes to be an active virus again! This latency might sound nearly identical to lysogeny in bacteriophages, and while it is quite similar, latency in mammalian viruses is much more rare, with herpesviruses and retroviruses being the only two substantial cliques of peek-a-boo fanatics among them.

EBV is spread effortlessly via bodily fluids including blood and saliva, hence its “kissing virus” moniker. But EBV can be acquired just as easily by sharing toothbrushes, utensils, food, or drinks! When EBV is latent, virus is not being churned out by our resident cellular virus factories to any detectable extent, and consequently a carrier of latent EBV (that is: most of us) is unable to spread the virus. But EBV is quite the surprise-party enthusiast, and if reactivated decades later, can begin to be spread yet again, even though our handy-dandy immune systems’ “second time is the charm” mentality keeps us from having outward symptoms.

Plus, symptoms of Mononucleosis vary drastically, but also typically include fatigue, sore throat, and swollen lymph nodes. Some symptoms can keep an individual bedridden for several weeks, but others might not trigger any perceptible symptoms. And even though most Mono cases persist for 2-4 weeks, others can take up to 6 months.

But keep yourself safe and healthy, by keeping your toothbrush and your fork to yourself and  the smooching to uninfected persons!