it's caused by a poor immune system. The things to bolster the immune system help put it into dormancy.
The drugs are known to cause kidney failure. There is no drug that is "anti virus" -- the drugs work by being cytotoxic to cells that are dividing. It is difficult to find studies on this of course because of how the system works but they are out there.
Acyclovir is what this review discusses, but it is really the same as the others mentioned as Valtrex is converted to it in vivo and the others probably work exactly the same:
Acute kidney injury due to acyclovir
Acyclovir is an important antiviral agent in the therapy of herpes simplex and varicella zoster virus infections [6]. Although the drug is well tolerated, severe nephrotoxicity, which often leads to acute renal failure, has been observed in patients [4, 7]. Acyclovir-induced renal failure occurs in approximately 12–48 % of cases [4]. The optimal usage of acyclovir is very important in order to avoid its potentially life-threatening complications. Acyclovir-induced nephrotoxicity is typically evident by an increase in the plasma creatinine level, abnormal urine sediment, or acute renal injury [8]. Acyclovir is rapidly excreted in the urine via glomerular filtration and tubular secretion, and reaches high concentrations in the tubular lumen. Renal excretion of unchanged drug reaches approximately 60–90 % [7, 9, 10]. Acyclovir is relatively insoluble in the urine, particularly in the distal tubular lumen [7, 9–12]. Rapid intravenous administration of high-dose acyclovir is associated with high luminal concentrations of this drug and the intratubular precipitation of crystals can cause renal injury [7, 9, 10]. Typically, crystalluria develops within 24–48 h of the initiation of acyclovir therapy. Severe intraparenchymal precipitation of crystals can cause interstitial congestion and hemorrhage, leading to a decrease of renal blood flow [7, 10–12]. The serum creatinine levels of our patient also began to rise within 48 h of acyclovir treatment. Renal biopsy revealed no sign of precipitation of crystals. Clinical evidence of nephrotoxicity in the absence of crystalluria was suggested to be secondary to the direct cytotoxicity effect of the drug to tubular cells and acute interstitial nephritis in our patient, as mentioned in other studies [8, 13, 14]. Renal biopsy findings of patients with acyclovir toxicity include bulging of tubular cells, dilated tubular lumens, loss of proximal–distal tubular differentiation, flattening and vacuolization of epithelial cells, and epithelial cell mitoses [8, 14]. A moderate and patchy tubulointerstitial infiltration of inflammatory cells and focal necrosis of cortical proximal tubules with edema were noted in our patient.
The administration of high doses of acyclovir (≥1500 mg/m2 per day) with other nephrotoxic agents, pre-existing renal disease, and dehydration play important roles in acyclovir nephrotoxicity [15]. Acyclovir dose should be reduced in patients with underlying renal insufficiency. Furthermore, slow drug infusion, over 1–2 h, adequate fluid replacement, and induction of high urinary flow rates (100–150 ml/h) should be encouraged in order to prevent crystal precipitation and subsequent tubular obstruction [7, 9–11, 16]. Despite vomiting 4–5 times a day as a predisposing factor for prerenal failure in our patient, she was adequately hydrated and no clinical evidence of hypovolemia was observed. Furthermore, any drug that causes nephrotoxicity was not used with acyclovir therapy.
I went to the doctor finally a few hours ago and he prescribed me valtrex. 1000 mgs 2 times a day.
He said to do this for 7 days then stop taking it...I'm afraid to drive to work in the morning (I drive a hour on the highway both ways for work) they say be carefull operating a vehicle because valtrex can possibly causes dizziness and effect motorskills as side effect. I can't take a week off either before christmas. I hate taking unatural medicine.