The inauguration of novel treatment strategies into the clinical setting faces a number of hurdles. In addition to treatment efficacy and safety, acceptance by doctors and patients is paramount to the success of novel therapies. Although viruses are the cause of numerous infectious diseases, these acellular entities have been harnessed over the years to benefit mankind. Recently, a recombinant Poliovirus-Rhinovirus Chimera (PVSRIPO) has shown promise for the treatment of glioblastoma in clinical trials as well as other cancer types in animal models. In this literature review, we discuss the use of PVSRIPO as an oncolytic virotherapy. In addition to being a potential treatment for glioblastoma, this recombinant virus could possibly be used against other cancers because many tumor cells express the PVSRIPO receptor antigens (CD155) and have a limited ability to control viral replication. Moreover, virus-induced immune responses contribute to the efficacy of PVSRIPO. Given the current trajectory of this experimental therapy, the possibility exists that PVSRIPO will soon be a viable treatment option for various cancer types. While many healthcare providers and cancer patients likely welcome this new viral based treatment, history has taught us that some may be skeptical and avoid its use because of the viral composition of this therapy.
Viruses are obligate parasites and can only reproduce within host cells because they lack metabolic pathways to complete their replication cycles.Host factors required in viral replication are mainly those involved in lipid metabolism, cell cycle control and apoptosis, cell-to-cell interactions, immune system regulation, etc.Several inhibitors targeting viral polymerases have been designed.However, the rapid appearance of resistant mutants, as a direct consequence of the viral population structure, diminishes the efficacy of this kind of molecules.To elude the rapid loss of treatment efficiency due to the appearance of resistance mutations, cellular factors have been proposed as a promising therapeutic target to inhibit RNA(+) virus replication.In this review, we focus on those interactions between host factors and HCV replicase, to modulate either cellular metabolism or HCV polymerase activity.
Primary infections caused by rubella and Cytomegalovirus (CMV) can front-runner to thoughtful complications in pregnancy. Rubella and CMV screening of adult women is not consistently conceded out in Bangladesh. The aim of this study was to determine the prevalence of rubella infection among CMV IgG sero-positive adult women. Throughout this study we reviewed the testing records of CMV IgG sero-positive adult women aged of 17-36 years who presented by random at immunology laboratory records at Dhaka Hospital Ltd., Bangladesh. Between January, 2014 to July, 2014, 51 anti-CMV IgG positive adult women were included and retrospectively evaluated in this study. The mean age of the selected CMV IgG sero-positive adult women in this study was 24.67±5.46 years. The highest sero-positivity for the anti-CMV IgG (15, 41.2%) and anti-Rubella IgG (14, 37.25%) were documented in 22-26 age group and followed by 29.4% for CMV IgG and 27.45% for Rubella IgG in 17-21 age group. The mean CMV IgG titer was 289.49 IU mL-1 for 17-21 age group while 99.03 IU mL-1 in Rubella IgG titer, 248.65 IU mL-1 CMV IgG titer for 22-26 age group whereas 103.21 IU mL-1 Rubella IgG, 275.06 IU mL-1 CMV IgG titer and 116.36 IU mL-1 Rubella IgG titer for 27-31 age group and 301.60 IU mL-1 CMV IgG titer although 109.76 IU mL-1 Rubella IgG titer for 32-36 age group. The median of CMV IgG titer and Rubella IgG titer were 233.80 IU mL-1 and 68.20 IU mL-1 with 298.00 and 126.90 IU mL-1 of 75% percentile respectively. Although high prevalence of CMV IgG and Rubella IgG were found (41.2 and 37.25%) in 22-26 age group, but the highest mean CMV IgG titer (301.60 IU mL-1) found in 32-36 age group while highest mean Rubella IgG titer (116.36 IU mL-1) was found in 27-31 age group. So, Deterrent actions must be taken to lessening the mortality and morbidity related to congenital rubella and CMV infections in fetus. The rubella and CMV status should be investigated before pregnancy and sero-negative females can be recommended for vaccination.
Avian metapneumovirus (aMPV) causes acute respiratory infection in turkeys with sudden onset and rapid spread in the infected flocks. Vaccinated flocks frequently showed clinical signs typical like the non-vaccinated flocks in Egypt, this situation suggests a virulent vaccine virus was circulating in the field. Oropharyngeal and nasal sinus swabs were collected from 100 turkeys from 10 commercial farms with mild to moderate respiratory signs. Virus isolation and propagation was done in SPF embryos of chicken eggs via yolk sac inoculation and further passed in Vero cells. RT-PCR for detection of aMPV was done on field samples as well as on virus isolates. Genotyping of viruses was done through RT-PCR targeting Fusion (F) and the surface Glycoprotein (G) genes and partial sequencing of PCR products was used for genetic and phylogenetic analyses. The results were compared with two live attenuated commercial vaccines commonly used in the field. Analysis of nucleotide and amino acid sequences for F and G genes indicated that they were very closely related to each other and belonging to B subtype of aMPV isolated from Europe. The Egyptian viruses were very close to VCO3 vaccine strain, indicating their possible origin. Phylogenetic analysis indicates clustering of the Egyptian field viruses with European strains of B subtype. These results support that they may have a common progenitor from vaccine strains and suggesting evidence of reversion of attenuated vaccine virus to virulence. This is the first report describing the emergence of vaccine-derived mutants from the B subtype aMPV in broiler turkeys in Egypt.
Many viruses, including DNA and RNA viruses, can persistently replicate in the infected cells and cause a prolonged damage. Herpes viruses can be latent in its host cells. Human Immunodeficiency Virus (HIV) reversely transcripts its RNA genome to DNA and integrates to the host’s chromosome. Hepatitis B Virus (HBV) and Human Papilloma Virus (HPV) persistently stay in the host cells as an episomal form, their genomic DNAs can also be integrated to the host’s chromosomes. Viral persistent infection is the major cause of the mortality among infectious diseases.
