Abstract
Human metapneumovirus (HMPV) is one of the leading causes of respiratory diseases in infants and children worldwide. Although this pathogen infects mainly young children, elderly and immunocompromised people can be also seriously affected. To date, there is no commercial vaccine available against it. Upon HMPV infection, the host innate arm of defense produces interferons (IFNs), which are critical for limiting HMPV replication. In this review, we offer an updated landscape of the HMPV mediated-IFN response in different models as well as some of the defense tactics employed by the virus to circumvent IFN response.
Highlights
Human metapneumovirus (HMPV) genomic organization resembles that of the respiratory syncytial virus (RSV) with the exceptions of lacking the non-structural proteins (NS1 and NS2) and of having a slightly different gene order (Figure 1)
The HMPV genome, which is constituted of approximately 13,330 nucleotides, encodes 9 proteins represented in the order
Data from two different studies indicate that HMPV was detected in nasal-wash samples of 12% of all lower respiratory infection (LRI) cases in a cohort of more than 2000 previously healthy outpatient infants and children [26], as well as in the respiratory aspirates of 12 (6%) of the 208 children hospitalized for acute respiratory tract infection (ARTI) [24]
Summary
Human metapneumovirus (HMPV) is a clinically relevant single stranded RNA virus that belongs to the genus Metapneumovirus in the new virus family Pneumoviridae [1,2,3]. 30 -N-P-M-F-M2(1/2)-SH-G-L-50 , and includes the nucleoprotein (N), phosphoprotein (P), fusion (F), small hydrophobic (SH), attachment (G), polymerase (L), and matrix proteins (M1 and M2), for which. Functional characterization of the HMPV viral proteins indicates that the virus fuses with the host cell membrane using the F protein [7]. The G protein contributes to the attachment of the virus to the host cell membrane, but is dispensable for virus replication [9]. The small hydrophobic (SH) protein has been reported to modulate membrane fusion promotion [10], its functional role in viral infection is still unknown. The phosphoprotein (P), nucleocapsid (N), and viral polymerase (L) are essential proteins for viral RNA synthesis [6,10,11]. HMPV has been classified into two main groups, i.e., A and B, and further subdivided into A1, A2, B1, and B2, based on genetic analysis [8,13,14,15]
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