Neither drug affected latency if treatment was delayed for several months. See also
Penciclovir
Valaciclovir

References
External links
Famvir product website run by Novartis
This would confirm that more than a single allele mutation is needed for the abnormal cell proliferation. KRIT1 has been shown to act as a transcription factor in the development of arterial blood vessels in mice. CCM2 has overlapping structure with CCM1 (KRIT1) and acts as a scaffolding protein when expressed. Both genes are involved with MAP3K3 and thus appear to be a part of the same pathway. CCM2 has been shown to cause embryonic death in mice. Lastly, the CCM3 gene has been shown to have similar expression to CCM1 and CCM2, suggesting a link in its functionality. Currently, no experiments have determined its exact function. The lack of function of these genes in control of a proliferative signaling pathway would result in uncontrolled proliferation and the development of a tumor. In 2018, it was theorized that proliferation of endothelial cells with dysfunctional tight junctions, that are under increased endothelial stress from elevated venous pressure provides the pathophysiological basis for cavernous hemangioma development. Diagnosis
Gradient-Echo T2WI magnetic resonance imaging (MRI) is most sensitive method for diagnosing cavernous hemangiomas. MRI is such a powerful tool for diagnosis, it has led to an increase in diagnosis of cavernous hemangiomas since the technologys advent in the 1980s. The radiographic appearance is most commonly described as "popcorn" or "mulberry"-shaped. Computed tomography (CT) scanning is not a sensitive or specific method for diagnosing cavernous hemangiomas. Angiography is typically not necessary, unless it is required to rule out other diagnoses.