Web Historical Disclaimer

This is a historical page and is no longer maintained. Read more information about historical pages and sites hosted by the university.

Cover Story



Virus 101

A primer on how viruses operate, mutate and wreak havoc
in your immune response

Written by Karen Krakower Kaplan and Samuel Kaplan, PhD

A year ago last spring, a new virus invaded our collective consciousness with such force that it shook the economic crisis off the front page.

It continued to scurry along the bottom of our TV screens, take up residence on Page One and spread like, well . . . a virus across our Web sites. Acronyms like “CDC” entered our daily lexicon; “WHO” no longer was a question. Never before had our hands been so clean and our elevator etiquette so polite. Masks and sanitizers were the new party favors and“social distancing” was the new cool. Aside from horrific misinformation that fanned absurd discrimination against Mexican citizens specifically and the swine industry in general, Novel H1N1 looked like it might burn off in the summer sun and head south for the winter like other flu viruses. We had hoped that with its initial low mortality rates, it would be remembered as a whoa-that-was-close cautionary tale.

So much for that.

As predicted by epidemiologists (those intrepid disease detectives), virologists and infectious disease experts, Novel H1N1 (novel, as in brand new version of H1N1) boomeranged back this flu season. In fact, it never really left at all.

So, why couldn’t we just kill it? When it comes to any virus, why can’t we take a pill, a bunch of pills, a vaccine, flame thrower, back hoe to the thing and crush it? What makes a virus so . . . viral?

cross-section illustration of virus

Most of the seasonal flus that affect us are the A strains: H1N1, H2N2, H3N2. The clandestine sounding code letters and numbers stand for the two proteins, hemagglutinin and neuraminidase, that are found on its surface; the numbers denote the protein form.

First, you have to know a bit about micro-organisms. There are more of them than there are of us and there are more of them living on and in us than there are people on the planet, sand on the beach, dollars owed to the deficit. There are more micro-organisms in our bodies than cells that make up our bodies! We are such walking Petri dishes of yeast, bacteria, viruses and fungi that we might ask ourselves, Who am I, really? (And, why am I not dead yet?) The simple answer: Because 99.99 percent of micro-organisms fall into one of three categories: friends, harmless hitchhikers– or guys that just aren’t that into us.

Then there is that nano-sliver of a percent left over: viruses like hepatitis, HIV, Ebola. They’re mean. Among the most common viruses is flu. Available in A, B and C flavors, influenza virus is the lyrical surname for the Orthomyxoviridae family that affects birds and mammals, with exotic nicknames like Brisbane or Hong Kong. Most of the seasonal flus that affect us are the A strains: H1N1, H2N2, H3N2. The clandestine-sounding code letters and numbers stand for the two proteins, hemagglutinin and neuraminidase, that are found on its surface; the numbers denote the protein form.

A virus, such as Novel H1N1, is an entity comprised of proteins (the H and the N), the basic component of all living systems, and nucleic acid, where bits of genetic information are stashed. But, for a virus to synthesize, grow in numbers, produce offspring, it needs additional machinery from a living cell. This is one of the primary differences between a virus and a bacterium: A bacterium usually brings its own copy machine, ink and printer; a virus mooches off a living cell’s material, then commandeers the cell and finally destroys it.

Viruses also are quite agile. From 100 to 1,000 times smaller than your average bacterium, they slide through the blood stream and slip through cell walls unnoticed.They’re also resourceful. The coat of each virus type is outfitted with a receptor that fits uniquely – like a key –to a specific lock. Novel H1N1’s receptor fits quite nicely with bronchial or pulmonary cell “locks.” Rhino viruses that cause the common cold have keys that open the lock to cells in the sinus passages. Though secondary infections requiring antibiotics can be created by opportunistic bacteria, the initial infectious agent was a virus, with the right key to the right lock.

Once the virus has unlocked the cellular door and made itself at home, eviction is tough. Unless our bodies’ defenses have met this virus before and have sentries on standby ready to attack, they’re likely to be caught off guard. By the time your white cells, lymphocytes, leukocytes and macrophages realize there’s an enemy in their midst and have begun to mobilize their various armed forces for attack, the virus has replicated so much that it has taken over the field (the lungs, the liver, the nose, etc.). When the “viral load” gets that high, it’s a numbers game.

Pigs of a feather

Why was H1N1 causing such a stir? Isn’t it just another similar viral strain that we’ve seen before, like this season’s newest Little Black Dress? Whether it’s bird flu, swine flu, human flu, isn’t it just flu? Sort of. But not really.

Viruses affect and infect all sorts of animal species –birds, (from whence all “flew” virus originated), horses, pigs, humans, etc. In the case of Novel H1N1, something unique happened: an avian flu, a swine flu and a human flu gathered in a pig cell for a genetic swap meet. What emerged was a “triple-reassorted” virus –a brand new strain made up of scraps from three old strains from three different creatures. Because our human bodies, including our immune systems, have never seen this new brand of virus, we are more prone to be sickened by it should we be exposed.

Flu, along with many (but not all) other viruses is transmitted from droplets breathed out, sneezed out, coughed out or handed out by someone carrying around a viral load of yuck. If you are in the contagious stage of the flu (the period from around 36 hours before symptoms to about seven days after) and you sneeze into your hand and then wheel a grocery cart around, the cart handle has your germs. The next person to touch that cart may then rub her eyes, wipe her nose, touch her mouth. Within a few incubatory days, the shopping cart germs have long since entered her respiratory system, hijacked a slew of cells, replicated exponentially and she not only feels ill, but has spent the last few days exposing her family without knowing she’s sick. You, however, may be on the healing end, but still “shedding” a trail of virus particulates.

Built for battle

Regardless of the species of germ – bacteria, virus, fungus – our bodies are designed to fight off foreign invaders. And, we respond really swell, thank you. If our immune systems come across an unknown assailant, it sets about manufacturing specific antibodies to fight it. And, for a reasonable time period, months to years, these antibodies stand on the ready to defend our bodies should we become exposed to that particular strain of virus again.

Science has given us some weapons over the years to augment our natural defense mechanisms. Antibiotics compliment our own immunities to fight off bacterial infections. Vaccines are our primary manufactured defense against viruses.

The modern vaccine is generally a soup of weakened (attenuated) virus particles. These bits and parts of the virus surface serve as mug shots on a viral Most Wanted List so that our immune systems can recognize them and begin to form a targeted defense should we find ourselves exposed to the real thing. We get our vaccines a few months ahead of flu season so that we have time to manufacture enough antibody protection to fight off an influenza infection. Since three or four predominant flu strains make up the fall collection circulating each year, you need the newest flu vaccine against those types.

Timing is critical. If you wait too long to get the vaccine, you could be exposed to the flu before your internal armies have time to report to duty. If you get it too early, your immunities could have worn off by the time the season’s in full swing.

The anti-viral medications for flu are the correlate to the antibiotics against bacterial infection. Neither of them kill their corresponding germs; they simply make it harder for germs to reproduce, which in turn gives our bodies’ defenses a leg up.

Should you still subscribe to the I’m-too-healthy-for-a-shot philosophy and whammo, find yourself in midstride feeling like you’re on fire (and not in a good way), your doctor might start you on an anti-viral medication, depending on the strain of flu and your unique health portrait. Taken within the first 48 hours while the virus is starting to bivouac, these drugs can stem viral replication enough to let your body’s defenses catch up.

For most of us, however, our doctors will recommend that we let our bodies’ natural defenses mount an attack.You’ll run fever (a byproduct of being in fightin’mode), you’ll be congested (your body’s attempt to trap and kill the virus) and you’ll ache all over (inflammation caused by the virus). If it’s a gastrointestinal virus, you may have vomiting and diarrhea (your body’sattempt to exorcise the demon). Sometimes, we become critically ill, due in part, to “friendly fire.” Our own immune system creates such havoc in an effort to destabilize the intruder that it destabilizes the host: Us. That’s when viral damage can turn deadly.

For the most part, the newest bully on the block, Novel H1N1, has proved to be wildly contagious, multi-seasonal and an equal-opportunity infector. H1N1’s total U.S. death toll may be as high as 17,000, according to the U.S. Centers for Disease Control and Prevention, compared to 36,000 a year for seasonal flu. The vaccine coupled with a massive public health campaign was by all counts, a successful defense.

This fall, who knows? Viruses are always changing, mutating – just trying to compete for survival. H1N1 may change just enough to fool our bodies’ defenses.Or, it may have a recurring role as an “also ran” seasonal strain, having lost its star power. We’ll have to wait and see – seems the virus holds that key.

It was a Friday afternoon in April, the last full day on a Caribbean cruise. Luis Ostrosky, MD, and his family were about to port in Cozumel, Mexico, when he caught a CNN report confirming suspicions of a ‘novel virus, never seen before.’ The same day, Robert ‘Safety Bob’ Emery, DrPH, picked up disturbing chatter on a public health list-serv citing a new swine flu strain that was dotting the North American map with clustered outbreaks.

Emery, vice president of environmental health and safety at The University of Texas Health Science Center at Houston (UTHealth), began putting together a posse of first responders to ride out ahead of the outbreak. The UTHealth team included members in infectious disease, public health, emergency medicine, clinical care, biosecurity, public affairs and administration.

The first order of business was to create a communication plan and essential messaging to inform, prepare and protect the 13,000 people on campus. Their second, should H1N1 become the 21st century’s 1918 plague, was to plan for a surge of patients.The Flu Preparedness Committee met by conference call the next morning to hammer out the plan’s scaffolding. The main message had to spread faster than the virus: simple hygiene.

“It was back-to-the-basics: How to wash your hands. How to stop the spread of germs,” recalled Ostrosky, who serves as associate professor of medicine and epidemiology in the Division of Infectious Diseases at UTHealth Medical School. “Sometimes, the simplest preventions are truly the best.”

By Monday morning, a team of writers and Web developers created a Web-based media resource and the Flu Center, an online information clearing house to allay fears, answer clinical and procedural questions,and address institutional issues ranging from antiviral availability to time-off policies for employees caring for flu-struck family members.

Susan Parnell, director of UTHealth’s Employee Health Services and a faculty member at the UTHealth School of Nursing, took the lead in counting, allocating and scheduling distribution of masks, gloves and Tamiflu stockpiles. Others began inventorying other critical equipment, such as flu testing kits and respirators.

As implications surrounding H1N1 grew, a second conference call was added to include world-renowned disease detectives such as Joseph McCormick, M.D., and Susan Fisher-Hoch, M.D., from UTHealth School of Public Health Brownsville regional campus and Houston’s Kristy Murray, D.V.M., Ph.D., whose Student Epidemiology Intelligence Society assisted city and county health departments with suspected cases of the virus.

“Early on, it was apparent that the virus was out pacing the city and county’s abilities to test for it, fill out the paperwork and track it,” Fisher-Hoch recalled. “We went over to Hidalgo and Cameron County to help and they were overwhelmed.”

Murray said, “Being on the ground at the health department afforded us the opportunity to track the first cases in Houston and predict where the virus was going and how it was spreading. Up until then, we did not know how contagious it was, how it affected patients, if it was weak, strong, lethal, light.” Later, Murray and students would travel to Mexico, believed to be ‘groundzero’ for the outbreak.

By midweek, a phone line had been installed for employees to report illness or to ask questions. Fitness for Duty guidelines were established for healthcare workers and employees who might fall ill. Administrative leadership drafted business continuity plans to keep the university’s engine running if whole departments fell ill.

UT Physicians, a clinical arm of UTHealth, mobilized supplies and carved out clinical space for patients presenting with flu symptoms. To protect the health of clinical providers, “fit-testing” of the medical protective gear was scheduled.

“We rallied quickly and performed more fit tests in those first two weeks of the outbreak than we perform in a given year,” Emery said. With response plans underway, Emery, Murray, Fisher-Hoch, Ostrosky and other university experts conducted dozens of interviews with media outlets, including CNN and the Associated Press, to educate the public about the health threat. Within seven days, UTHealth had done what it set out to do: inform, prepare and protect. “We’re a weathered group, when it comes to rapid mobilization,” Emery said.

“We’ve earned our stripes at being able to take the lead in times of crisis – from hurricanes and floods to pandemic preparation. We know how to take care of our own in a heartbeat.”

Karen Krakower Kaplan

Karen Krakower Kaplan is director of University Communications & Publications and is editor of HealthLeader Online Magazine.

Samuel Kaplan

Samuel Kaplan, Ph.D., is professor and chair of the Department of Microbiology and Molecular Genetics/UTHealth Medical School