The role of intestinal protozoa in chronic obstructive pulmonary disease exacerbation.

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with episodes of exacerbation. Variable factors including infectious pathogen can predispose for this exacerbation. The aim of this study is to evaluate the role of intestinal protozoa in COPD exacerbation. A total of 56 patients with COPD were included in this study. Patients were categorized into two groups based on the frequency of exacerbation during the last 6 months: those with ≤1 exacerbation (32 patients) and those with ≥2 exacerbations (24 patients). Stool specimens from each patient were collected two times (one week interval) examined for intestinal parasite. In univariate analysis, rural residence and parasitic infection were more common among patients with frequent exacerbation (45.83% and 33.33%, respectively) than patients with non-frequent exacerbation (18.75% and 9.38%, respectively) with significant differences. However, in multivariate analysis, only body mass index >25 kg/m2 (OR=4.59, 95%CI=1.18-17.86, P=0.028) and parasitic infection (OR=5.51, 95%CI=1.01-30.18, P=0.049) were independently associated with COPD exacerbation. These data indicate a significant association between frequent COPD exacerbation and infection with some intestinal protozoa. However, the cause-effect relationship is debatable.

Phylogenetic analysis of human pegivirus from anti-hepatitis C virus IgG- positive patients.

Human pegivirus type 1 (HPgV-1) is a non-pathogenic RNA virus in the Flaviviridae family that usually occurs as a co-infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), though some evidence suggests it may play a role in certain cancers. The present study aimed to determine the prevalence of HPgV-1 infection in Iraqi anti-HCV IgG-positive patients, the risk factors associated with this infection, and the genotype of local isolates of this virus. A total of 88 anti-HCV IgG-positive patients participated in this cross-sectional study. Viral RAN was extracted from whole blood samples, and cDNA was produced using reverse transcriptase-polymerase chain reaction (RT-PCR). Two pairs of primers were used in nested PCR to amplify the virus genome's 5'-untranslated region (5'UTR). For direct sequencing, fourteen PCR products from the second round of PCR were chosen at random. A homology search was performed using the basic local alignment search tool (BLAST) program to identify the resultant sequencing. The phylogenetic tree of the local isolates and 31 reference isolates was constructed using MEGA X software to estimate the virus's genetic diversity and relatedness. Out of 88 patients included in this study, 27(30.68%) of patients were found to be positive for HPgV-1 RNA. The nucleotide homology between the 14 local isolates and the reference isolates. was found to be 87-97%. Phylogenetic analysis results in a tree with four main parts, which are distributed as follows: 10 local isolates are genotype 2; 2 are genotype 1; 1 is genotype 5, and 1 is genotype 6. We conclude that when compared to other countries, the infection rate of Iraqi anti-HCV IgG-positive patients with HPgV-1 is relatively high (30.68%). The most common HPgV-1 genotype in Iraq is genotype 2.

The role of cytotoxic T-Lymphocyte antigen-4+49A/G gene polymorphism in cutaneous leishmaniasis.

BACKGROUND: Cutaneous Leishmaniasis (CL) is a parasitic disease caused by intracellular protozoa belonging to the Leishmania genus. In endemic areas, only a proportion of exposed subjects develop the disease under almost similar circumstances, reflecting the role of genetic inheritance in resistance and susceptibility to infection. This study aimed To evaluate the association of cytotoxic T-lymphocyte antigen-4 (CTLA-4)+49G/A single nucleotide polymorphism (SNP) with incidence and severity of CL. METHODS: This cross-sectional study includes 110 patients with confirmed CL (60 newly diagnosed and 50 patients undergoing treatment) and 60 healthy subjects of similar age and sex. The CTLA-4 gene fragment corresponding to CTLA-4+49G/A polymorphism was amplified and genotyped using tetra primer amplification refractory mutation- polymerase chain reaction system (TARMS-PCR) methods. Soluble CTLA-4 (sCTLA-4) was estimated in the serum using an enzyme-linked immunosorbent assay (ELISA). RESULTS: The GG genotype of CTLA-4+49G/A polymorphism was significantly more common in controls than in patients (OR = 0.11, 95% CI = 0.02-0.58, p = 0.009). At allelic level, G allele was much more common in controls than in patients (30.83% vs. 17.73%) with a significant difference (OR = 2.07, 95% CI = 1.23-3.48, p = 0.006). However, there was no significant difference in the frequency of genotypes and alleles between newly diagnosed and treated patients. Median serum concentration of sCTLA-4 in newly diagnosed patients was 72.6 pg/ml (range 15.6-127 pg/ml) which was higher than either controls (median = 16.3 pg/ml, range 0.8-48.5 pg/ml) or treated patients (median = 17.9 pg/ml, range 2.9-74.7 pg/ml) with highly significant differences, while there was no significant difference between controls and treated patients. The median sCTLA-4 level was comparable across genotypes of the CTLA-4+49G/A polymorphism, with no significant difference. CONCLUSIONS: Collectively, these results show the protective role of allele G of the SNP CTLA-4+49G/A against CL and increased serum sCTLA-4 in newly diagnosed CL patients, which may be used as an additional diagnostic tool. Different genotypes of the CTLA-4+49G/A polymorphism have no effect on sCLTA-4 serum levels.

Association of ABCB1 gene polymorphism (C1236T and C3435T) with refractory epilepsy in Iraqi patients.

The mechanisms of refractory epilepsy (RE) are most likely multifactorial, involving environmental, genetic, as well as disease- and drug-related factors. We aimed to study is to investigate the possible association of two ABCB1 gene polymorphism (C3435T and C1236T) with the development of RE in Iraqi patients. One hundred patients with either generalized tonic-clonic seizures, myoclonic epilepsy, or absence epilepsy comprised of 60 patients responsive to AEDs and 40 patients who were refractory to treatment who used multi AEDs for at least one month were studied. Fifty family-unrelated age- and sex-matched healthy subjects represent the control group. ABCB1 gene fragments corresponding to two targeted polymorphisms were amplified with conventional polymerase chain reaction using specific sets of primers. Genotyping was performed by restriction fragment length polymorphism (RFLP) technique. Epileptic patients refractory to AEDs showed a significantly higher frequency of CC genotypes of C3435T polymorphism than controls. Allele C was significantly higher in patients than controls and far more frequent among patients with RE. C1235T polymorphism had no significant role neither in the incidence of epilepsy nor in the AEDs resistance. The CT haplotype was more frequent among patients refractory to AEDs. In contrast, the haplotype block TT was more frequent among responsive (41.3%) than refractory patients (28.7%) (p = 0.068). The CC genotype and C allele of the C3435T polymorphism can increase the risk of RE. The haplotype block CT of C3435T and C1236T can predispose for epilepsy as well as the drug resistance.

Association of BCR/ABL transcript variants with different blood parameters and demographic features in Iraqi chronic myeloid leukemia patients.

BACKGROUND: Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of BCR-ABL fusion gene (GenBank accession NC_000022.11). In the vast majority of CML patients, the typical subtype of BCR-ABL transcript are b3a2, b2a2 or both. The aim of this study was to determine the different subtypes of BCR-ABL transcript and their impact on the demographic and hematological parameters in Iraqi patients with CML. METHODS: One hundred patients with chronic phase CML (11 newly diagnosed and 89 imatinib-resistant) were enrolled in this study. Ribonucleic acid (RNA) was extracted from leukocytes, and complementary DNA was created using reverse transcriptase polymerase chain reaction technique. A multiplex polymerase chain reaction with four specific primers was used to determine the BCR-ABL fusion subtypes in each patient. RESULTS: Male to female ratio was 1.38:1. Fifty-nine patients expressed b3a2 transcript, whereas 39 of the remaining cases were positive for b2a2 variant. One case expressed b2a3 transcript, while the last case coexpressed the two subtypes of mRNA b3a2/b2a2. Male and female were significantly associated with b3a2 and b2a2 subtypes, respectively. The b3a2 subtype showed higher total leukocyte count than b2a2 subgroup, while b2a2 variant demonstrated significantly elevated platelet counts compared to those with b3a2 transcript. A significantly higher plateletcrit percentage (PCT%) was found in patients with b2a2 transcript whereas. CONCLUSIONS: The testified Iraqi group expressed M-BCR-ABL type with preponderance of b3a2 over b2a2 subtype. There was a gender-skewed distribution in BCR-ABL transcript types with b3a2 transcript more prevalent in males. The type of BCR-ABL transcript is reflected by different leukocyte and platelet counts at diagnosis, which might represent a distinct phenotype and disease biology.

Genotyping of Cytomegalovirus from Symptomatic Infected Neonates in Iraq.

Among all other viruses, human cytomegalovirus (HCMV) is the most frequent cause of congenital infection worldwide. Strain variation in HCMV may predict severity or outcome of congenital HCMV disease. Previous studies have associated a particular genotype with specific sequelae or more severe illness, but the results were contradictory. There are no previous studies addressing the genotype of HCMV in Iraq. Therefore, the present study is aimed at molecular detection and genotyping of HCMV isolated from symptomatic congenitally/perinatally infected neonates. This prospective study comprised 24 serum samples from symptomatic neonates with congenital/perinatal infection. Viral DNA was extracted from these serum samples; nested polymerase chain reaction was used to amplify the HCMV gB (UL55) gene. Polymerase chain reaction products of the second round of amplification were subjected to direct Sanger sequencing. Bioedit and MEGA5 software (EMBL-EBI, Hinxton, Cambridgeshire, UK) were used for alignment and construction of a phylogenetic tree. Human cytomegalovirus DNA was detected in 23 of 24 samples (95.8%). According to the phylogenetic analysis, three genotypes of the virus were identified; gB1, gB2, and gB3 genotypes. However, the gB4 genotype was not detected. Human cytomegalovirus gB3 was the most frequent genotype: 14 of 24 (58.33%) among symptomatic infected infants, followed by gB1 (6/24; 25%) and gB2 (4/24; 16.67%). A mixed HCMV infection with gB3/gB1 was detected in only one case. Human cytomegalovirus gB3 was the most predominant genotype among symptomatic congenitally/perinatally HCMV-infected neonates. No association was found between B3 genotype and specific clinical presentation. Jaundice was the most common clinical feature among symptomatically infected neonates, followed by hepatosplenomegaly.