The development and use of vaccines against some serious
human viruses was certainly one of the great success stories of 20'th century
biological science. In the early decades of the 20'th century, viral diseases
such as yellow fever, polio, and rabies were greatly feared, because there was
no effective way of preventing the very serious diseases caused by these easily
transmissible viruses. The development of new vaccines remains one of the main
goals of much virology research.
1. What are the available vaccines against human viral
diseases, and what are some updates on the use and effectiveness of these vaccines?
The main human viral vaccines, roughly
in order of when they were developed, are:
VIRUS/DISEASE VACCINE TYPE
Smallpox Live Vaccinia virus (Led
to the global elimination of smallpox by late 1970's.)
Yellow fever Live
attenuated strain (of yellow fever virus)
Measles Live attenuated strain
(of measles virus)
Mumps Live attenuated strain (of
mumps virus)
Rubella Live attenuated strain
(of rubella virus)
Polio Live attenuated strain (Sabin) or Inactivated virions (Salk) (2007 JID article )
Influenza Inactivated virions or live attenutated strain ( NEJM articles, December 2006)
Rabies Inactivated virions (for
post-exposure use)
Hepatitis B Viral envelope glycoprotein
(from cloned HBV DNA)
Varicella-zoster Live attenuated strain (1990's) (March 2007 update, NEJM article)
Hepatitis A Inactivated virions (1990's)
Rotavirus Live attenuated strain (2006 article) & human-bovine reassortment strain (2006 article)
HPV Virus-like particles ( NEJM perspective 2006)
2. What is an end-of-2006 update on influenza vaccine effectiveness?
See these three articles from December 2006 NEJM:
Editorial: Different Approaches to Influenza Vaccination
Article: Prevention of Antigenically Drifted Influenza by Inactivated and Live Attenuated Vaccines
Article: Effectiveness of School-Based Influenza Vaccination
In general, attenuated live vaccines are longer lasting and produce both
humoral and cell-mediated immunity, whereas inactivated or sub-unit vaccines
produce only humoral immunity. A risk factor for an attenuated
live vaccine strain, however, is the possibility that it could genetically revert back to being pathogenic. This
is an important issue, because this situation actually took place (albeit
very rarely) for the live polio vaccine. So, we ask ....
3. For polio, how different genetically is the attenuated
viral strain (the Sabin vaccine) from the wild-type virulent strain (that causes
paralysis)? What is the genetic structure of one rare revertant strain that
arose from the vaccine strain several decades ago?
As shown here, the Sabin vaccine strain is different from
the wild-type "Leon" virulent strain at only 10 of the 8000 nucleotides
of the poliovirus genome.
Administration of the Sabin strain to many millions of children resulted in virulent revertant strains causing paralytic disease at a frequency of about 1 child in 4 million. One such revertant strain that arose from the vaccine strain is different at only 9 nucleotides (here). Comparing the two figures shows that at only one of these sites (nucleotide position 472) is the revertant change the exact reversal of the original attenuation change.
