Culex pipiens is the most widely distributed mosquito species in the Maghreb and is suspected to be involved in WNV and RVFV transmission. Using experimental infections, we showed that Cx. pipiens populations collected in Algeria, Morocco and Tunisia were highly susceptible to infection and readily to transmit WNV and to a lesser extent, RVFV.
To be transmitted to a vertebrate host, an arbovirus must be able to reach and infect the salivary glands. After feeding on a viremic vertebrate host, the ingested virus must penetrate into the midgut epithelial cells, replicates and subsequently, escape from the midgut. The virus disseminates within the body cavity infecting tissues and organs including salivary glands. Infectious viral particles are injected into a new vertebrate host along with saliva. Barriers to the overall sequence leading to transmission are described: the midgut and the salivary glands (reviewed in 
). The efficiency of these barriers determines the level of mosquito vector competence. For both viruses tested, WNV and RVFV, the time interval between the ingestion of a viremic blood-meal and the ability of a mosquito to transmit a pathogen, described as the extrinsic incubation period (EIP) was 3 days with Cx. pipiens
from Tabarka (Tunisia).
When exposed to an infectious blood-meal containing WNV, all mosquito strains collected in 8 different sites in the Maghreb, were capable to ensure efficient viral dissemination and transmission at day 14 pi. Our findings are in line with the predominant role of Cx. pipiens
in the transmission of WNV. DIRs varied from 59% to 100%, and TRs from 25% to 100%. The number of viral particles delivered with saliva was up to ~ 12800 particles. Vector competence is mainly influenced by viral dose, incubation period and temperature. We used a viral titre of 107.8
PFU/mL and an incubation temperature of 28°C, both factors affecting viral dissemination 
. Indeed, the minimal infectious doses required to infect Cx. pipiens
should be greater than 105.0
and high temperatures increase viral replication 
. Previous studies have shown spatial variations in WNV vector competence of Cx. pipiens
. We also observed geographic variations in vector competence without assignment of high performances to a given country or a collection site.
We used for RVFV, the Clone 13 which is a naturally attenuated strain with a deletion of 70% of the gene NSs playing a key role in the pathogenesis of RVFV 
. It has been shown that this deletion could affect viral replication in mosquitoes. It has been shown that dissemination was higher when exposed mosquitoes to a virulent RVFV 
. We found that 14 days after exposure to RVFV, 69.2% of mosquito strains were able to develop a disseminated infection with DIRs up to 38.1%, values higher than those previously found for Cx. pipiens
populations from Tunisia 
but lower than DIRs for laboratory colonies of Cx. pipiens
. Most strains (77.8%) were able to transmit the virus with up to ~ 620 viral particles detected in saliva. The midgut infection was the most important barrier to viral dissemination 
. The moderate ability of Cx. pipiens
to transmit RVFV is mostly due to the inefficiency of virions to escape from midgut epithelial cells to infect secondary target organs 
. When increasing the incubation period up to 21 days, 78.6% of mosquito strains develop a disseminated infection and 91% were able to deliver infectious particles in saliva. Thus, Cx. pipiens
with disseminated infection that did not have infectious saliva at day 14 pi may have viral infections to develop a week later 
. Moreover, the midgut barrier appears to be operating by delaying the release of the virus into the general cavity of Cx. pipiens
infected with RVFV 
. A sporadic dissemination of virus from the midgut was likely to operate rather than a complete blockade of the virus inside the midgut epithelial cells.
Our strains contain a mix of autogenous (AU) and anautogenous (AN) mosquitoes. The two forms are thought to have different vector competences (reviewed in 
). Indeed, we found evidence that when challenged with RVFV, AU mosquitoes were predominantly capable to ensure the viral dissemination and transmission, 14 days after the exposure to the infectious blood-meal (see ). Surprisingly, AN mosquitoes were characterized by a delay in RVFV transmission; AN populations were more likely to transmit 21 days after feeding on an infectious blood-meal (see ). We suggested that epizootic outbreaks of RVF can be initiated by Aedes
mosquitoes which are present in high densities in rural areas 
mosquitoes such as Ae. vexans
in West Africa 
capable to transmit the virus vertically to their offspring are likely to initiate the virus circulation. Subsequent epizootic outbreaks are associated with Culex
mosquitoes. Based on their low vector competence, we hypothesized that AN mosquitoes in rural areas weakly take part to RVFV transmission. AU mosquitoes are more likely to serve as a bridge vector between animals and humans. A RVF cycle could then be initiated when AU mosquitoes reach densities high enough to trigger an epidemic/epizootic outbreak. The Maghreb region shares borders with RVF-endemic countries. In 2010, a severe outbreak has been reported in an extremely arid region of Mauritania close to borders with Morocco and Algeria 
. Introduction of infected livestock raised concern for future emergences of RVF. Indeed, the RVF outbreaks in Egypt in 1977 and in Saudi Arabia in 2000 were caused by the trade of viremic animals 
Like WNF, RVF could become epizootic and epidemic in the Maghreb if introduced. Unless vaccines are available and used on a very large scale to limit their expansion, both WNF and RVF will continue to be a critical issue for human and animal health. In a near future, protection of the public health will continue to rely on mosquito control. Further studies are required to understand the bio-ecology of Cx. pipiens and other mosquito vectors in the Maghreb.