Peste des petits ruminants virus infection of small ruminants: a comprehensive review

Abstract

Peste des petits ruminants (PPR) is caused by a Morbillivirus that belongs to the family Paramyxoviridae. PPR is an acute, highly contagious and fatal disease primarily affecting goats and sheep, whereas cattle undergo sub-clinical infection. With morbidity and mortality rates that can be as high as 90%, PPR is classified as an OIE (Office International des Epizooties)-listed disease. Considering the importance of sheep and goats in the livelihood of the poor and marginal farmers in Africa and South Asia, PPR is an important concern for food security and poverty alleviation. PPR virus (PPRV) and rinderpest virus (RPV) are closely related Morbilliviruses. Rinderpest has been globally eradicated by mass vaccination. Though a live attenuated vaccine is available against PPR for immunoprophylaxis, due to its instability in subtropical climate (thermo-sensitivity), unavailability of required doses and insufficient coverage (herd immunity), the disease control program has not been a great success. Further, emerging evidence of poor cross neutralization between vaccine strain and PPRV strains currently circulating in the field has raised concerns about the protective efficacy of the existing PPR vaccines. This review summarizes the recent advancement in PPRV replication, its pathogenesis, immune response to vaccine and disease control. Attempts have also been made to highlight the current trends in understanding the host susceptibility and resistance to PPR.

Figure 1

Genome organization of peste des petits ruminants virus (PPRV). Negative-stranded PPRV genome (RNA) containing 15,948 nucleotides and six genes that encode eight proteins. At the 3' and 5' ends there are untranslated regions (UTRs) of 52 nt and 37 nt, respectively. The terminator region of each gene is followed by a three nucleotide-long conserved (GAA) region called intergenic region (IG). IG region is also found at the junction of leader sequences and the N gene (first gene) and between the L gene (last gene) and the trailer region. Each transcription unit (to produce individual viral protein) is composed of the coding sequence(s), IG region and the conserved start and stop signals that flank the coding sequence(s). Besides the full length P protein, the open reading frame (ORF) of the P gene also produces two non structural proteins, namely C and V by alternative reading frame (leaky scanning) and RNA editing, respectively. IG = intergenic region, N = nucleocapsid protein, M = matrix protein, F = fusion protein, H = hemagglutinin protein, L = Polymerase (large) protein. Number indicates the length of nucleotides of the individual gene.

Figure 2

PPRV life cycle. (1). Attachment of the virus to host cell receptors (SLAM/Nectin-4) via its HN protein. (2). Fusion with plasma membrane via the F and HN proteins (3). Release of the viral genome into cytoplasm. (4). Genome replication by the virus-encoded RdRp of the RNPs (5). mRNA synthesis by the virus-encoded RdRp in the ‘start-stop’ mode (a mechanism of controlling the amount of individual protein being produced). (6). Synthesis of full-length positive sense RNA (antigenome RNA or complementary RNA, cRNA). (7). Synthesis of viral proteins: F and H proteins are synthesized on RER (7A1) and translocate across Golgi complex (7A2), where post-translational modifications take place. Other viral proteins (N, P, C, V, M, L) are synthesized on ribosomes (7B). (8). Assembly of progeny virions. (9). Budding of the progeny virions at the plasma membrane.