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Establishment of a PPR Global Research and Expertise Network (PPR-GREN)

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Date:
Wed, 5 Feb 2014 13:06:27 -0500
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rabindra singh <[log in to unmask]>
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rabindra singh <[log in to unmask]>
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"Establishment of a PPR Global Research and Expertise Network (PPR-GREN)" <[log in to unmask]>
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Dear Paul,
We are the one at Indian Veterinary Reserach Institute, who developed the Monoclonal antibodies and also related diagnostic kits and the vaccines. We have reasons to believe that PPR virus may be a little less stable as compared to rinderpest virus. Reasons for it are different/ 4- lineages of PPRV, distributed across the globe. I do not know if these many number of lineages were present in Rinderpest virus. I further believe that a single strain of rindepest vaccine virus ie RBOK strain was sufficient enough for mass vaccinations and Rinderpest Eradication through out the globe. As for as reactivity of monoclonal antibody is concerned, it may be lost even with the single point mutation in the nuleotide critical for that epitope. We have sucessfully, generated mab resistant mutants from vaccine/original viruses which do not react with the anti "H" mabs. But escape from a polyclonal sera , which has antibodies aginast several epitopes, is some thing which can not be explained. I fully agree with your view that , it/escape from vaccinated/polyclonal antibody is not normally expected out of a morbillivirus. There are resons to believe, that PPRV lineage-4 has spread in several parts/countries of Africa recently (Albina-2013), and these countries were believed to have only lineage 1,2, &3. It is also possible that viruses belonging to other lineages i.e. lineage1,2,&3 may be present in Asia now/not frequently reported. These findings can be proved only when organized molecular epidemiology is caried out in this/ Asian region. Futher, there has been sufficient molecular epidemiological investigations upto year 2002 and not beyond that period. India mainly focussed on seroepidemiology on several occassions between the year 1999 to 2010. As for as vaccine efficacy is concerned, there are success stories of about gradual reduction/decline of PPR outbreaks to the tune of 99% ( 1 outbreak as against more than 200 outbreaks) in some of the administrative units/ states of India using this (Sungri strain) vaccine.

Based on my experiences from Rindepest eradication in India (I was involved in Final stage of Rinderpest sero-surveillance and Eradication while working at Muktswar campus) and also PPR control program, I believe that, once PPR is controlled in Primary hosts/ small ruminants by mass vacciations, the antibodies from other hosts (cattle /bufflo camel) will aoutomatcally disappear over a period of time. These may not interfere with the final stage of PPR eradication, as has happened with rinderpest. Even though it may be difficult to maintain high flock/herd Immunity in case of PPR due to high foecundity of small ruminants/ dynamic population.
regards,
Dr. R.P.Singh, 
Principal Scientist, Division of Biological Products,
Indian Veterinary Research Institute, Izatnagar, 
Bareilly-243 122 (Uttar Pradesh),
India

Alternate email: [log in to unmask]
Mobile:+91-9412360917
----- Original Message -----
From: Paul Rossiter
Sent: 02/05/14 07:13 PM
To: [log in to unmask]
Subject: From Dr Naveen Kumar on interesting molecular and antigenic characteristics of an isolate of PPRV , concerns about PPR in cattle plus moderator's comments

----- Forwarded Message -----
From: Naveen Kumar <[log in to unmask]>
To: Paul Rossiter <[log in to unmask]>
Cc: [log in to unmask]; [log in to unmask]
Sent: Tuesday, 4 February 2014, 7:41
Subject: E-conference on progressive control of PPR

Dear All,

I am working as a Senior Scientist in an Institute in India working specifically for goats "Central Institute for Research on Goats, Makhdoom, Mathura, India". I have been involved in activities like attending filed outbreaks of PPR/pox and isolation and characterization of the field strains. I would like to share my experience and seek your suggestions on the followings:

1. We, isolated a PPR strain from an outbreak in goats. The PPRV that I isolated has following properties. In repeated attempts, the virus was not captured in Antigen ELISA, developed by Indian Veterinary Research Institute, Mukteshwar and it very poorly reacted with monoclonal antibodies as well as hyperimmune serum raised against Indian vaccine strain (Sungri96). Moroever, the PCR amplification of H and F genes was unsuccessful with at least 11 different pairs of primers (note that side by side the vaccine strain gave expected amplification with each pair of primer). However, the virus agglutinated the chicken RBC (Hemagglutination) and exhibited CPE on third blind passage in Vero cells characteristic to that of a Morbillivirus (fusion, syncytia, degeneration). Later, the nucleoprotein (N) gene which is considered as quite conserved among different strains was also successfully amplified. About 327 nucleotide long PCR product (N gene) was gel purified and sequenced. When the sequences were BLAST it completely matched with PPRV (Accession Number DQ267191). Certainly this is PPR virus but does not cross react with the monoclonal antibodies and hyperimmune serum vaccine strains. What it suggests ? I understand that in beginning when the homologous vaccine against PPRV was not available, a heterologousrinderpest virus vaccine was used for control PPR suggesting a cross protection among Morbillivirus exists even in distantly related viruses (PPRV/rinderpest) so the cross protection should also occur at least within PPRV strains. In my opinion this might not be the case. We should carefully look how the virus is changing itself in the natural environment. I have attached the manuscript of these finding which published recently in J. Virological Methods.

Clearly this is an important observation that needs clarification. I hope that some of our molecular and monoclonal wizards in this conference will comment here. In the meantime I would like Dr Kumar to tell us whether the goat from which he isolated this virus had been vaccinated with Sungri vaccine (since, unless I am mistaken, the inference is that this might be a virus that evades this vaccine - -which is not something that is usually expected with morbilliviruses, and definitely not something that we want). Furthermore, how was the outbreak that yielded this virus brought under control? Through vaccination and if so with which vaccine? I shall try to distribute the J Virol Meth paper to all participants if they haven't received it already. Moderator.

2. The rinderpest caused an acute disease in cattle whereas the sheep and goats undergo subclinical infection. However as we all know that the PPRV only cause subclinical infection in cattle but a clinical disease and hence a high mortality in sheep and goats. Scattered reports of isolating PPRV from animal species other than sheep and goats is not necessarily that the prevalence of the infection in cattle is low; it may be due to the fact that we are attempting the virus isolation only from the animal (sheep and goats) clinically affected. Attempting virus isolation particularly from the cattle which is in close vicinity from an infected sheep and goat herd is likely to show more evidence of infection in cattle. In rinderpest control programme, only cattle and buffalo were the target species for mass vaccination (not sheep and goats). Assumption have been made that the PPRV emerged from rinderpest virus by natural passage (subclinical infection) in sheep and goats. Now the question here is whether or not to include the cattle in mass vaccination campaign, while launching progressive control of PPR. A live attenuated vaccine probably may not be suggested for cattle but an inactivated vaccine may be attempted ( though its not economically viable). Continuous natural passage of PPRV in cattle may lead to emergence of new PPRV like virus in cattle ?

A couple of points. One is that PPRV did not emerge following natural passage of rinderpest virus in sheep and goats. PPRV is significantly different to RPV and evolved from a common ancestor hundreds or thousands of years ago. Other more knowledgeable colleagues can help me here. Two, I agree that we need to know more about the behaviour of PPRV in cattle, domestic buffaloes and other susceptible species. But the main issue is: can these species maintain the virus independently of small ruminants thereby becoming of epidemiological significance? Answering this question should be one of the main reasons for further study in these species. I don't know the absolute zero-risk answer but I haven't seen any evidence to suggest that they can maintain the virus. Attempting to isolate virus from clinically normal cattle in close proximity to PPR affected sheep and goats might yield something interesting but will be a very expensive exercise especially when measured against all the other research and control interventions that will require funds from what I suspect, will always be a limited pot of money. Years ago during cattle plague in northern Pakistan we isolated RPV from a sheep showing very mild clinical and pathological signs of rinderpest. I was sure that having crossed the species barrier the virus would spread amongst the sheep and goats in that village. I was wrong. When we looked at sheep and goat sera from the village a month or two later, hardly any animals had antibody. In other words the RPV had not spread in the sheep and goats and the infected animal that we examined clinically and then at post-mortem was very unlucky. Moderator.

Thanks and regards
NaveenKumar

--
Naveen Kumar, BVSc&AH, MVSc,PhD
Senior Scientist (Veterinary Virology)
Room No.118, Division of Animal Health
Central Institute for Research on Goats
Indian Council of Agricultural Research
Makhdoom, PO-Farah-281122 
District-Mathura, UP
India
Tel: +91 565-2763260 Ext 269
 +91 08171301889 (cell)
Fax:+91 565-2763246
email:  [log in to unmask] web: http://www.cirg.res.in/goat_health.php 

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