My name is Siamak Zohari and I’m researcher at the National Veterinary Institute (SVA) in Sweden. We at the SVA together with colleagues from Mozambique are involved in European founded project; IUEPPR (coordinated by prof. Satya Parida, The Pirbright Institute (PI), Pirbright, UK). In this project we are trying to deal with several aspect of PPR including improved understanding of the epidemiology of peste-des-petits ruminants.
First of all I would like to thank you all for sharing your experiences and for all valuable input. I agree with many of you that the e-conference has facilitates many exchange and giving us a nice opportunity to learn more about the experiences from field situations and also nice overview over the laboratory activities in regards to vaccine and diagnostic developments and different DIVA approaches.
 
Several points regarding vaccine:
                            
1-      It not clear to which immune effectors can be correlated protection following vaccination: Systemic neutralising  and non-neutralizing antibodies, mucosal immunity, cytotoxic T cell, etc. You are right, we probably do not know the exact effectors of vaccine induced immunity to PPR, but we do know that it works and that vaccinated animals, like recovered animals, are solidly immune.  We know that antibodies are involved because of the passive tranfer of immunity in colostrum, which is well documented for PPR, and also from rinderpest where the use of serum to modify infection was one form of vaccination a  century or more ago. There are papers on the effect of specific anti-PPRV serum inoculated in small ruminants.   We also know from rinderpest, (assumptions of course) that cattle that had been vaccinated or recovered from infection 8 or more  years earlier and had subsequently become completely or almost antibody negative (neither very  common)  resisted challenge with live virus. All these cattle showed a strong anamnestic neutralising antibody response. Whether the immunity was due to the anamnestic response or to cell-mediated immunity is unknown but they were immune.
 
2-      I would also like to raise the question on immunological memory and long term immunity in regards to PPRV infection. The generation of specific Immunological memory is indeed the most important requirement/purpose of prophylactic vaccination. How long is the immune memory following vaccination in Sheep and goat? It is assumed that it is lifelong following the use of live vaccine in sheep and goat with so many vaccine formulations but is it right?  I do not have all my papers to hand but the PPRV vaccine induces immunity for several years and there are publications which show that it probably lasts longer than the life of most small ruminants. In rinderpest (again - sorry) vaccinated cattle from Zanzibar (where they had never been challenged by field virus to boost their immunity) were immune to challenge after twelve or was it fourteen years?
 
3-      The spread of different lineage of PPRV in to new geographical locations and indication by molecular epidemiological studies of co-circulation of several lineage of PPRV in the same geographical locations (in ex. lineage 2, 3 & 4 in Tanzania) highlights the need for confirmation of whether the commercial available vaccines from one of the lineages (such as lineage II-Nigerian 75/1) could protect against PPRV from each of the known genetic lineages of the virus separately and in situation with co-infection of the individual animal with different lineages at the same time. How much is the cross protection between lineages? Our knowledge about the duration of the specific neutralizing antibodies after vaccination against homologus and heterologous challenge is limited. Although the humoral responses tend to correlate with level of protection from clinical disease there might be a difference between level of protection between homologus and heterologus challenge.  The level of clinical and virological protection through the duration of immunity following vaccination is probably influenced by the antigenic difference between vaccinal and field strains.  This could explain that some vaccinated animals can shed virus absence or slight clinical signs. For this reason the evaluation of the duration of immunity in sheep and goat following vaccination need to be evaluated with homologous and heterologous PPR strains.    This seems to be a very tenacious subject.  I am sure that monoclonal antibodies will distinguish strains of PPRV but I do not know of any major antigenic differences between strains of PPRV and currently this virus is considered to have one serotype.  Vaccine strain Nig75/1 and other vaccines developed in South Asia can be expected to protect against all genetically defined lineages.    I reckon that scientists and field staff working to control many other infectious diseases still plaguing the world would be only too willing to swap their vaccine (if they have one ) for ours. - Moderator.  
 
Best Regard
Siamak
 
Siamak Zohari, Msc, PhD
Department of Virology, Immunobiology and Parasitology
National Veterinary Institute (SVA) &
OIE Collabraiting Center
-for Biotechnology-based Diagnosis of Infectious Diseases in Veterinary Medicine
Ulls väg 2B, SE-751 89 Uppsala
Phone: +46-18-674106, +46-702573263
Fax: +46-18-674669