Water with entrained disease-causing virus entering soil normally passes through water saturated and unsaturated regions before reaching the groundwater. Twelve experiments were conducted to evaluate the effect of saturated versus unsaturated flow, and the effect of organic matter in unsaturated flow on the survival and transport of a virus, MS-2 bacteriophage, in soil columns. Additional experiments were conducted to characterize the soil, to assure that the experimental equipment did not remove virus, and to determine the extent of reversible adsorption of virus to soil. The virus were added to well water and applied to soil columns 0.052 m in diameter and 1.05 m long. KBr was used as a chemical tracer. In two experiments organic matter in the soil water was increased by using soil humic material or extract from sewage sludge. The soil material was Vint loamy fine sand (a sandy, mixed, hyperthermic Typic Torrifluvent) mixed with recent alluvium. Water samples were extracted from 0.10, 0.20, 0.40, and 0.80 m depths through porous stainless steel samplers, and from the 1.05 m depth through the percolate tube. Four different eluants were tested to remove virus from soil, and one, tryptic soy broth, was used to elute virus after three transport experiments. For saturated flow the virus concentrations reached the influent concentration in less than 2 pore volumes (T), with a retardation coefficient R at 1.05 m = 0.80. For unsaturated flow with low organic matter the relative concentrations reached steady-state values (C/C₀)(s) ranging from a mean of 27% of inflow at 0.20 m (5 to 18 T) to a mean of 5% at 1.05 m (1 to 3.3 T). Under unsaturated conditions with increased organic matter, virus (C/C₀)(s) at 1.05 m was from 41% to 49% of influent, 8 to 10 times greater than with low organic matter. Elution permitted calculation of a partition coefficient k(p) essentially equal to 0 (saturated average k(p) = -0.07 mL/g, SD = 0.15 mL/g; unsaturated average k(p) = 0.28 mL/g, SD = 0.40 mL/g), indicating little or no adsorption of virus to soil solids. Under unsaturated flow conditions enhanced removal of this virus occurs, and the removed virus are apparently inactivated. Organic matter reduced the removal of virus during transport by unsaturated flow. Virus concentrations reached and maintained a steady-state, exponentially-declining profile with depth.

Recently a new Flavivirus, GB Virus C also referred to as Hepatitis G virus (GBV-C/HGV) was identified in humans with indeterminate hepatitis . Whilst in non-African countries this discovery led to an enormous enthusiasm to elucidate an association with liver disease, very little was known about the prevalence and pathogenicity of GBV-C/HGV infection in KwaZulu Natal, South Africa, where Hepatitis B Virus (HBV) infection is endemic and infection with the Human immunodeficiency virus (HIV) is a catastropic health problem. Sera from patients with liver disease (chronic liver disease [n = 98]; alcoholic liver disease [n = 50]); high risk groups (haemodialysis patients [n = 70]; HIV positive mothers and their babies [n = 75]) and control groups (alcoholics without liver disease [n = 35] and blood donors from the four racial groups [n = 232]) were screened for GBV-C/HGV RNA and Anti-E2 antibodies by reverse transcription polymerase chain reaction (RT-PCR) and an enzyme linked immunosorbent assay (ELISA), respectively. Overall 43.9% (43/98) of patients with chronic liver disease; 60 % (30/50) of patients with alcoholic liver disease; 47.1% (33/70) of haemodialysis patients; 60% (21/35) of alcoholics without liver disease and 31.9% (74/232) of blood donors (Africans] 44/76; 5.9%); Asians (5/52; 9.6%); Whites (15/49; 30.6%) and "Coloureds" [mixed origin] (9/54; 16.6%)]) were exposed to GBV-C/HGV infection as determined by the detection of Anti-E2 &/or RNA in serum. There was a significant difference in the prevalence of GBV-C/HGV infection (RNA &/or anti E2) between African blood donors and the other racial groups (p < 0.001), between blood donors and haemodialysis patients (p = 0.02) and or patients with chronic liver disease (p =0.04). There was no significant difference in the prevalence of GBV-C/HGV between African blood donors (45/76, 59.2%) and alcoholics with and without liver disease (30/50, 60% and 21/35, 60%, respectively). Anti-E2 antibodies and GBV-C/HGV RNA were almost mutually exclusive. GBV-C/HGV infected dialysis patients tended to have had more transfusions (p = 0.03) and had a longer duration of dialysis than non infected patients, indicating that the majority of patients on maintenance haemodialysis acquire their GBV-C/HGV infection through the transfusions they receive. There was no evidence for in utero and/or intrapartum transmission of GBV-C/HGY. However, there is some mother-to-infant transmission of GBV-C/HGV, though it is very probable that in KZN GBV-C/HGV is transmitted by as yet undefined non-parenteral routes. Sequence and phylogenetic analysis of the 5' non-coding region (5' NCR) and E2 gene segments of the GBV-C/HGV genome identified an additional "genotype" (Group 5) of GBV-C/HGV that is distinct from all other known GBV-C/HGV sequences (Groups 1-4). Although there is a high prevalence of Group 5 GBV-C/HGV isolates in KZN, there was no significant difference in liver biochemistry between GBV-C/HGV infected and noninfected patients with liver disease or between blood donors in each of the four racial groups. There was no significant differences in CD4 (461.12 ± 163.28 vs 478.42 ± 181.22) and CD8 (680.83 ± 320.36 vs 862.52 ± 354.48) absolute cell counts between HIV positive patients co-infected with GBV-C/HGV and those not infected with GBV-C/HGV, respectively. However, significantly higher relative CD3 [80.0 ± 4.17% vs 70.99 ± 19.79%] (p = 0.015), gamma delta T cells (yLT) [3.22± 1.30% vs 2.15 ± 29.12%] (p = 0.052) and lower CD 30 [35.45 ± 17.86% vs 50.59 ± 9.20%] (p = 0.041) status were observed in GBV-C/HGV positive compared to GBV-C/HGV negative HIV infected patients, respectively. Although there is a high prevalence of novel Group isolates of GBV-C/HGV in KZN, the lack of elevated liver enzymes and clinical hepatitis in blood donors and haemodialysis patients suggests that GBV-C/HGV is not associated with liver disease. HBV and not GBV-C/HGV modifies the course of alcoholic liver disease. The relatively higher number of CD3 cells and increased yLT expression, together with a decrease in CD 30 cells tends to suggest an association with protection and or delayed progression of HIV disease in GBV-C/HGV infected patients. Whilst GBV-C/HGV is not associated with liver disease, it may be an important commensal in HIV infected patients. / Thesis (Ph.D.)-University of Natal, 2003.