Rift valley fever (RVF) is an acute vector-borne viral zoonotic disease of domestic and wild ruminants. The RVF virus (RVFV) belonging to the Phlebovirus genus of the Bunyaviridae family causes this disease. Studies have shown that mosquitoes are the vectors that transmit RVFV. Specifically, Aedes and Culex mosquito species are among the many vectors of this virus, which affects not only sheep, goats, buffalo, cattle, and camels but also human beings. Since the 30s of the last century, RVF struck Africa, and to a lesser extent, Asian continents, with subsequent episodes of epizootic, epidemic, and sporadic outbreaks. These outbreaks, therefore, resulted in the cumulative loss of thousands of human lives, thereby disrupting the livestock market or only those with seropositive cases. After that outbreak episode, RVF was not reported in Libya until January 13, 2020, where it was reported for the 1st time in a flock of sheep and goats in the southern region of the country. Although insufficient evidence to support RVF clinical cases among the confirmed seropositive animals exists, neither human cases nor death were reported in Libya. Yet, the overtime expansion of RVF kinetics in the Libyan neighborhoods, in addition to the instability and security vacuum experienced in the country, lack of outbreak preparedness, and the availability of suitable climatic and disease vector factors, makes this country a possible future scene candidate for RVF expansion. Urgently, strengthening veterinary services (VS) and laboratory diagnostic capacities, including improvement of monitoring and surveillance activity programs, should be implemented in areas at risk (where imported animals crossing borders from Libyan neighborhoods and competent vectors are found) at national, sub-national, and regional levels. The Libyan government should also implement a tripartite framework (one health approach) among the veterinary public health, public health authority, and environmental sanitation sectors to implement RVF surveillance protocols, along with an active partnership with competent international bodies (OIE, FAO, and WHO). Therefore, this review comprises the most updated data regarding the epidemiological situation of RVF infections and its socioeconomic impacts on African and Asian continents, and also emphasize the emerging interest of RVF in Libya
Abdusalam Sharef Mahmoud(12-2021)

The imprinted expression of the IGF2 and H19 genes is controlled by the imprinting control region 1 (ICR1) located at chromosome 11p15.5. This methylation-sensitive chromatin insulator works by binding the zincfinger protein CTCF in a parent-specific manner. DNA methylation defects involving the ICR1 H19/IGF2 domain result in two growth disorders with opposite phenotypes: an overgrowth disorder, the Beckwith– Wiedemann syndrome (maternal ICR1 gain of methylation in 10% of BWS cases) and a growth retardation disorder, the Silver–Russell syndrome (paternal ICR1 loss of methylation in 60% of SRS cases). Although a few deletions removing part of ICR1 have been described in some familial BWS cases, little information is available regarding the mechanism of ICR1 DNA methylation defects. We investigated the CTCF gene and the ICR1 domain in 21 BWS patients with ICR1 gain of methylation and 16 SRS patients with ICR1 loss of methylation. We identified four constitutional ICR1 genetic defects in BWS patients, including a familial case. Three of those defects are newly identified imprinting defects consisting of small deletions and a single mutation, which do not involve one of the CTCF binding sites. Moreover, two of those defects affect OCT-binding sequences which are suggested to maintain the unmethylated state of the maternal allele. A single-nucleotide variation was identified in a SRS patient. Our data extends the spectrum of constitutive genetic ICR1 abnormalities and suggests that extensive and accurate analysis of ICR1 is required for appropriate genetic counseling in BWS patients with ICR1 gain of methylation.
Demars, J., Mansur Ennuri Moftah Shmela, S. Rossignol, J. Okabe, I. Netchine, S. Azzi, S. Cabrol, C. Le Caignec, A. David , Y. Le Bouc, A. El-Osta , C. Gicquel(9-2010)

On March 2013, the Libyan poultry industry faced severe outbreaks due to mixed infections of APMV-1 (Newcastle disease) and low pathogenic avian influenza (AI) of the H9N2 subtype which were causing high mortality and great economic losses. APMV-1 and H9N2 were isolated and characterized. Genetic sequencing of the APMV-1/chicken/Libya/13VIR/7225-1/2013 isolate revealed the presence of a velogenic APMV-1 belonging to lineage 5 (GRRRQKR*F Lin.5) or genotype VII in class II, according to the nomenclature in use. Three AI viruses of the H9N2 subtype, namely A/avian/Libya/13VIR7225-2/2013, A/avian/Libya/13VIR7225-3/2013, and A/avian/Libya/13VIR7225-5/2013, were isolated and found to belong to the G1 lineage. Analysis of amino acid sequences showed that the analyzed H9N2 viruses contained the amino acid Leu at position 226 (H3 numbering) at the receptor binding site of the HA, responsible for human virus-like receptor specificity. On March 2014, an outbreak of highly pathogenic avian influenza (HPAI) virus of the H5N1 subtype was diagnosed in a backyard poultry farm in an eastern region of Libya. The H5N1 isolate (A/chicken/Libya/14VIR2749-16/2014) was detected by real time RT-PCR (rRTPCR). Genetic characterization of the HA gene revealed that the identified subtype was highly pathogenic, belonged to the 2.2.1 lineage, and clustered with recent Egyptian viruses. This study revealed the presence of a velogenic APMV-1 genotype and of two influenza subtypes, namely HPAI H5N1 and H9N2, which are of major interest for public and animal health. Considering these findings, more investigations must be undertaken to establish and implement adequate influenza surveillance programs; this would allow better study of the epidemiology of APMV-1 genotype VII in Libya and evaluation of the current vaccination strategies.
Ibrahim Eldaghayes(5-2015)