Johnye writes:

Please see the particularly the section: Approach to the Infant with Suspected Intrauterine Infection

Begin forwarded message:

Subject: Overview of TORCH infections

A thumbnail sketch about TORCH infections from UpToDate. It may give some clinical information.

Reaching back from my newborn medicine pediatric point of view, TORCH titers were drawn when an infant was born with Intra-uterine growth retardation ( IUGR) or sick and appearing septic and blood cultures are negative or, perhaps infants sick and small for gestational age (SGA) or, if there were some stigmata of intrauterine infection or, in cases where the placenta appeared abnormal or suggested intrauterine infection.

From the obstetrical (OB) point of view, I imagine if intrauterine growth diminished or decelerated, perhaps TORCH titers would be ordered as part of a work-up.

OB and Neonatology TWiV listeners could comment more authoritatively.

Johnye Ballenger

Chris writes:

The comparison with congenital rubella syndrome was awesome.  Do not forget the devastation caused by other diseases spread by the same mosquito:  dengue and yellow fever.  The morbidity and mortality numbers for those make the stats for Zika seem very tiny.

The Aedes aegypti mosquito is not native to the Americas, so any method to eradicate them (including genetic modification) is fine by me.  I have had dengue fever, I don’t want it again.  I vote for any way to get rid of the little beasts.

Dear TWiVers, please refer to previous weather report by Barbara, since we are in the same city.  It is February in Seattle, therefore it is either raining or it is foggy.  My outerwear choices are either a sweater for the fog, or my poncho with sleeves for the rain.

Russ writes:

FYI, see report of pyriproxifen larvicide, not zika virus, as cause of microcephaly in Brazil. Doesn’t make sense in view of discussion on past two TWIV episodes, but I pass it along. Here’s the link:


Martin writes:


Why don’t you address the question I am trying to ask: why are you happily a part of a system that jumps the gun without proof! Fear and panic are the result. Even to the point of Obama requesting $1.8 billion to fight Zika. You–the academy–are the scientific authority. You have a responsibility here.

Martin “the broken clock who is right twice a day”

David writes:

Dear Twivniks,

What if you thought you sent your child off to college and they ended up on a cruise ship instead?  A physician friend of mine has a daughter at Ursinus College in Southeastern Pennsylvania.  She was one of the early victims of a recent norovirus outbreak:   

Apparently this kind of thing has happened in the not so distant past: e.g., three different campuses in 2008:

It makes one wonder whether college dining facilities, like cruise ships, need to be much more fanatical about sanitation.  Even if they were, the total environment (campus vs. ship) is much less controllable.  As is the target population.  Nevertheless, another opportunity for the Twiv bump.

If it takes more than ten episodes for a podcaster to have a shot at sustainability, how many does it take for a listener?  I’m a relative newcomer currently working on one hundred episodes or so.  I probably won’t ever get the chance to make my way through the archive.  But for me Twiv has now achieved the status of ritual and a very enjoyable and informative one, at that.  Remember that for humans the choice is never ritual or no ritual, but rather which ones.

Keep on twivvin’ and twimmin’ and twippin’ and …. (How many of you remember Robert Crumb),


David J. Spector, Ph. D

Professor Emeritus of Microbiology and Immunology

Penn State Hershey

Kevin writes:

Greetings Twivonauts,

I’m writing to clarify a couple of points about germinal center B-cells and to share a hypothesis about hemozoin and B-cell activation.

No one said anything incorrect about AID and germinal centers, but a couple of things might have been misleading. Alan said that during affinity maturation, B-cells that don’t get higher affinity get deleted. Though this is often the end result, it implies that there’s a way to sense an increase in affinity. In fact, germinal center B-cells are competing for activation signals, and there’s only so much to go around. The highest affinity B-cells get the most signal, and continue to proliferate – it’s like natural selection in miniature. If the initial B-cell receptor happens to have the highest affinity even after hypermutation, B-cells that retain it would get all the activation signals and survive.

The second thing is that you talked about AID in affinity maturation, and seemed to imply that sometimes this accidentally leads to breaks in the DNA that lead to translocations. Actually, there are rarely double stranded breaks in the antigen binding region of the BCR gene where hypermutation occurs. But AID is also responsible for the double standard breaks that are intentionally caused during class switch recombination. I haven’t kept up with the literature since my first year of grad school, but my recollection is that there are large g/c rich switch regions that get excessive C to U mutations that destabilize the chromosome.

Finally, Vincent said that we don’t know why hemazoin would increase AID expression in B-cells – I have a hypothesis. Many years ago, Shizuo Akira’s lab showed that hemazoin is a fairly potent activator of TLR9, which is normally thought of as a receptor for DNA. We also know that strong TLR9 signaling is able to activate B-cells even in the absence of T-cell help – it’s thought that SLE, an autoimmune disorder in which anti-DNA and anti-histone antibodies are often detected, may occur due to large quantities of self-DNA getting endocytosed by B-cells and aberrantly activating TLR9.

Perhaps hemozoin is triggering B-cells proliferation non specifically, and/or lowering the threshold for activation – since activation triggers AID transcription for somatic hypermutation and affinity maturation, maybe they’re not measuring increased AID expression by activated B-cells, but rather increased numbers of B-cells being activated.


Aarchan writes:

Hi Vincent,

On microcephaly… it’s a structural diagnosis as you know, with presumably many causes.

On its related eye manifestations:

On recent genetic mutations and eye involvement:

Microcephaly and anencephaly involve global growth dysregulation of the brain/skull… from an ophthalmic perspective, the brain is an organ involved in processing vision, so it’s reasonable to assume that in cases of widespread brain developmental abnormalities, there would be retinal and optic nerve dysfunction as well.

I communicate with Tatjana Avsic, the corresponding author on the NEJM article from last week… they looked at the brain, but not the eyes for Zika virions / genome — given that the virus is in the brain, it’s not a stretch to look for and likely find it in the eyes, alas, not so easy this time.



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