This review briefly discusses patterns of selected cytokine (IL-6, IL-8, IL-10, TNF-α and INF-γ) responses associated with infections caused by Plasmodium, intestinal parasites as well as a Plasmodium-helminth co-infection.
Other predictors for ESLD were older age, being of Sub-Sahara African descent, increased alanine aminotransferase levels and hepatitis C virus coinfection.
Furthermore, almost one third of the patients in the studied group was coinfected with transfusion-transmitted virus (TTV) and manifested significantly higher ALT levels (p = 0.020), and these were raised further if coinfection with TTV and human hepatitis C virus had occurred (p = 0.010).
Our findings further imply a convergent mechanism of inhibition of TLR signaling by <i>T. gondii</i> and IL-10 and suggest potential negative consequences of HIV/<i>T. gondii</i> coinfection.
Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection.
Antigens from the tapeworm Hymenolepis diminuta and the nematode Trichuris muris caused an anti-inflammatory response with M2-type polarization, reduced macrophage phagosome maturation and ability to activate T cells, along with increased Mtb burden, especially in T. muris exposed cells which also induced the highest IL-10 production upon co-infection.
An increase of messenger RNA (mRNA) expression of Th1- (IFN-γ, IL-12, TNF-α) and Th2-related cytokines (IL-10) mainly in groups PC-E and TE was observed, however, without statistically significant differences between co-infection and single infection with Eimeria.
Statistically significant univariate associations were observed between GBV-C-RNA positivity and younger age (P=0.006) and HCV-RNA positivity (P=0.024), as well as with higher serum alanine aminotransferase levels (P< 0.001); this latter association was shown to be independent of coinfection with HCV and of age by a multiple logistic regression model.
In multivariable analyses, the following factors predicted an ALT level >50 IU/mL: log10 HCV RNA (OR, 1.15; 95% CI, 1.00 to 1.32); HIV co-infection (OR, 0.48; 95% CI, 0.25 to 0.89); and having ever been treated for HCV (OR, 1.92; 95% CI, 1.16 to 3.18).
The spectrum of liver disease in coinfection includes a significant proportion of patients with normal ALT values, and excluding these patients from previous studies has led to an overestimation of HCV disease severity.
Our findings suggest that common IL-10 (-1082, -819 and -592) genotypes/haplotypes do not influence the degree of HAI and response to combination therapy or susceptibility to HCV infection with and without S. mansoni co-infection.
Furthermore, we studied the frequency of coinfection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) as well as a possible relationship to the alanine aminotransferase (ALT) status of the blood samples, taken at random from thalassaemic children who have received multiple blood transfusions and from volunteer blood donors.
Anellovirus was highly prevalent (93.3%) and the co-infection with multiple genera (alpha, beta, and gammatorquevirus) were more common in the donors with normal ALT values in comparison to those with elevated ALT (single/double/triple Anellovirus genera, 1/3/24 vs. 7/7/14 or 6/7/13, p = 0.009).
Among those with mixed infection, a significant proportion (44.2%) of CH-B patients, had ALT levels greater than the upper limit of normal (ULN), as compared with the blood donor groups (16.6%; p = 0.036).
These findings indicate that coinfection is associated with a type 1 IFN monocyte activation profile which was further found to correlate with cognitive impairment, even in subjects with controlled HIV infection.
The production of interferon (alpha-1 interferon [IFN-alpha 1], IFN-alpha 2, and IFN-beta), interleukin (interleukin 1 alpha [IL-1 alpha], IL-1 beta, and IL-6), and tumor necrosis factor alpha (TNF-alpha) mRNA was characterized by quantitative polymerase chain reaction mRNA phenotyping in U937 and U9-IIIB cells following coinfection with Sendai paramyxovirus or stimulation with lipopolysaccharide (LPS).
The findings suggest the possibility that co-infection by serologically-silent HBV is one of the factors that can lead to an unfavorable IFN response in chronic hepatitis C by down-regulation of IFN receptor gene expression in the liver.
An increase of messenger RNA (mRNA) expression of Th1- (IFN-γ, IL-12, TNF-α) and Th2-related cytokines (IL-10) mainly in groups PC-E and TE was observed, however, without statistically significant differences between co-infection and single infection with Eimeria.
HIV-1 infection did not stimulate constitutive production of endogenous IFN-alpha 1/alpha 2 or IFN-beta genes, although induction of IFN RNA was observed following coinfection with the paramyxovirus Sendai.