Posts Tagged ‘viral infection’

Say “Goodbye” to all of this . . .

June 4th, 2010

Greg and I moved back to our home in Vermont today.  Now, instead of weekly visits to the hospital in Boston, we’ll only have monthly visits.  This would’ve come much earlier had it not been for the (likely) false diagnosis of CMV and the myelosuppressive therapy that ensued, which may well have been key to my contracting the C. difficile that knocked me down so far.  But despite all of this, I’m now doing quite well and feeling very strong.

Last Tuesday during my last weekly visit, I was in the room where nurses take vital signs, and a woman was sitting next to me. She was wearing a mask and gloves, and when this sort of thing happens—when two transplant patients are sitting next to each other—there’s this strange E.T.-and-Elliot thing that goes on; we just want to talk to each other.  Or in my case: I can tell they’d like to connect with me, and I usually resist this, being a curmudgeon and all.  But on Tuesday, the woman sitting next to me just jumped right in.  She started asking me questions about my progress since transplant.  I was in a pretty good mood that day, but had this happened on practically any other day, I’d probably have perceived this as rude prying.  On this day, I saw it as tolerable prying, so we had a chat.  During our discussion, she asked me how far along I was since transplant.  I told her just over two months; she was quite surprised.  She went on to say that she was six months out, and that I looked so good she thought I might be nine or more months since transplant, but certainly ahead of her.

I was pretty surprised by this reaction, and it made me realize that I just didn’t have any frame of reference for how well I’m recovering relative to the average patient.  I’ve always thought that I’ve been doing pretty well, but I’ve never really known.  So I asked my physician what he thought.  He said emphatically that I was doing much, much better than most in terms of recovery, energy level, activity level, and such.  In fact, except for the uncontrollable neuropathy and my problems with the treatment for that (more on that later), I don’t have many complaints.  I’m more energetic now than I’ve been in ten years, and my red blood cell count is still rather low, but rising steadily, so more energy is yet to come.

So, despite my setbacks—the main one being the serious blow I took from the C. difficile—I seem to have rebounded and my health status has more than “caught up.”  My blood cell counts look great for my stage, and my physician has actually started tapering my immunosuppressives, a month or two early.  That means my lymphocytes will come on board earlier (but still many months away), which means protection from viruses.  But this could also mean that Graft Versus Host Disease (GVHD) is going to hit soon.  But GVHD also means Graft Versus Lymphoma effect:  All my cells are me, including any remaining cancer cells that are almost certainly floating around.  If—or rather, when my new immune system recognizes that it’s in a body of foreign cells and initiates an attack on my whole body, that attack will be on any remaining cancer cells too.  In fact, because this attack is mediated by T-lymphocytes—and those cells normally communicate with B-cells when they initiate an immune response—this means that when GVHD does hit, those T-cells will preferentially seek out B-cells during their attack on my body.  As I have B-cell lymphoma, those lingering cancerous B-cells will very likely come into contact with those T-cells that are seeking to fight off my cells.  When this happens, the T-cells will recognize that my B-cells are foreign too, and some of those T-cells can kill my cancer cells on the spot (so-called, Cytotoxic T-cells).

So, GVHD is kind of a mixed bag.  But one thing is certain from the empirical literature: Long-term survivors of stem cell transplants have mild-to-chronic GVHD.  These people are far less likely to relapse, and people who have no GVHD are far more likely to relapse.  So even though I’m over some serious infection hurdles, and even though the majority of death risk is clustered in the first three months post-transplant, I’m about to start facing the next challenges.

But I’m happy to be healthy, at least for now.  And Greg and I are both very glad to be home.  But I think we will both miss our deluxe apartment in the sky-hi-hi.  And just for memento, here are some photos of the view we’ve lived with for the last 75 days:

The Prudential Building (tallest), and a couple of others that no one cares about.

Christian Science weirdos. Despite being cuh-ray-zee, their buildings are "truly beautiful to behold," including this lovely library.

More Christian "Scientists," with their absolutely lovely buildings (all the buildings in view are CS buildings in the famed "Church Park.") The shadow cast is from our sixties-built, 1984-style 12-story building (not run by the Christian Scientists . . . as far as we know).

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There’s mono, and then there’s mono

May 27th, 2010

In an earlier post I discussed cytomegalovirus (CMV) primarily in relation to its impact on the immunosuppressed—people with AIDS and those of undergoing a stem cell transplant, for example. As a prelude to that discussion, I mentioned that CMV causes mononucleosis.  This piqued a reader’s interest:

. . .[I] found it interesting that CMV was related to mono—I’ve had mono, though apparently tested negative twice before positive, but am CMV negative—thankfully!

Presumably, the test for mono the reader mentions was a test for Epstein-Barr Virus, and not CMV. Epstein-Barr Virus (EBV) is another herpes virus that is closely related to CMV, and EBV causes a disease named infectious mononucleosis.  CMV causes a disease very similar to mono, and many authorities call that disease infectious mononucleosis.  The Centers for Disease Control says the disease caused by CMV is a “mononucleosis-like illness,” whereas the National Institutes of Health states flatly that both EBV and CMV cause mono.  When I took microbiology, I apparently learned virology from the NIH school of thought.  But it seems more authorities discuss EBV in relation to mono, perhaps because EBV is more likely to cause disease at initial infection (even though many show no symptoms), whereas CMV usually causes no or very mild symptoms in people when they catch it.  But both are attributed with causing a disease of the same name.  So why the hell is that?

First, it’s important to note that these two viruses are quite closely related—on the evolutionary tree of life, I mean.  And so EBV and CMV share essentially all of their genes, with some minor variations (minor for sure when compared to the total genetic diversity of life, or even that among viruses). Because of this, it is no surprise that they cause similar disease.

Second, it’s also important to keep in mind that viral nomenclature is a complete mess.  The international rules of nomenclature that have been well-established in zoology and botany for nearly a hundred years (but deriving from rules that are centuries old) are simply not in place for viruses.  The best recent example of this is the HIVs.  When Montagnier in France first isolated a virus he suspected to cause the plague of immunodeficiency that was killing off mainly gay men, he named it LAV (for Lymphadenopathy Associated Virus).  Then Gallo in the USA named it HTLV-III (for Human T-Lymphotropic Virus III)—and that name is now used for a completely different virus. The virus that causes what would be named AIDS was also called ARV (Adenopathy Related Virus) for a time.  Ultimately, yet another name was established by international convention (sort of): HIV. But now we know that the thing we call HIV is in fact at least two distinct groups of viruses that entered the human population via separate events.  What a shambles.

I only point this out because this confusion about viral nomenclature spills over into disease nomenclature.  Lots of named diseases—”the flu,” “the cold,” “AIDS”—are in fact each caused by many different, often closely related but nonetheless distinct species.  And this unfortunate practice is not restricted to viruses:  Human “malaria” is caused by one of four quite distinct microorganisms, and the characteristics of the diseases they cause are just as distinct.  This is all to say that the tiny creatures that cause disease evolve just like the bigger creatures they live in. Species split, become isolated, acquire mutations independently, get different, and ultimately become two species.  Although the new species did “get different,” they also share almost all of their traits by inheritance.  Whatever characteristics the initial, ancestral species had, the two new descendant species will very likely share most of those same characteristics.  In other words, close relatives are a lot alike because they come from common stock—something we all know from our own families.  And this is why two differently named viruses can cause the same named disease (even though, in a perfect world, virologists would stop this nonsense).

So the reader is right:  One can have a diagnosis of mono without CMV, and it’s CMV—not EBV—that is so problematic for those with trashed immune systems.  All important points of clarification for those who might be facing a stem cell transplant.

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Some not-so great news

May 12th, 2010

My last post was an honest and authentic expression of my thoughts and feelings about my current state of being.  I wasn’t hiding anything.  But there is something else going on.

This morning I awoke with a runny nose and some congestion.  This could be a minor bacterial infection, which would not likely be a problem to snuff out.  But, given that my mucus is clear, bacterial infection seems unlikely.  Viral infection is more consistent with that sign.  It could be one of a number of common viruses that cause runny nose.  For some of these, anti-viral treatments are available.  For many, the viruses don’t even have names, but they don’t cause dangerous infections either.  I’m hoping for one of these, of course.  It could be the flu, and (despite rapidly increasing resistance) that is treatable with osteltamivir.  But it could be something much more dangerous:  the seemingly innocuous, simple, common cold.

While the common cold causes the mildest of infection in immunocompetent people, in me, it could be a disaster.  Permanent scarring of the lungs is one outcome; death is another.  As no treatment for the common cold exists (though a number of experimental therapies are soon to help out), recovery relies on one’s immune system entirely.  Chicken soup may soothe, but it doesn’t cure.

Viral infections are defeated by lymphocytes.  The two main groupings of lymphocytes are T-cells and B-cells.  T-cells circulate in our blood, looking for proteins that are not self.  When one is found, the T-cell starts dividing, and some of those T-cells seek out B-cells.  The T-cells notify B-cells of the presumptive invader, and through one of the most amazing biological processes ever elucidated, germ-specific antibodies are produced.  Those antibodies ultimately cause cells infected with viruses to die (among other things).

So T-cells initiate (and later suppress) immune response.  B-cells primarily give rise to antibodies. The problem for me is that I don’t have very many of either of these cells.  Unlike neutrophils (white blood cells that primarily fight bacterial infection) and platelets, many developmental intermediates come between stem cell and mature lymphocyte, and it can take up to nine months for mature lymphocytes to appear after transplantation.  I do have a few lymphocytes from before the transplant, but it’s not clear that they will be of much use.

At this point, I just have to wait.  If matters get worse, I’ll get a nose swab tomorrow.  That might reveal a treatable virus or an untreatable virus.  Maybe I don’t have a virus.  I just don’t know right now, but in addition to being energetic and happy, I’m starting to get pretty scared.

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